Biology U4 AOS 1

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Last updated 10:47 AM on 9/27/26
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90 Terms

1
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  • What is the immune system responsible for?

  • Pathogens

  • Antigens + their forms

  • Antigens do not need to be attached to a pathogen or cell, they can simply be free-floating molecules. T or F?


  • The immune system protects our body by scanning for and destroying pathogens - disease causing agent that impairs the normal functioning of an organism 

 

Antigen: any molecule that can trigger an immune response in the body (short for antibody generator) 

  • Depending on their source, antigens can exist as many different types of molecules, including proteins (mostly), sugars, and DNA or RNA (nucleic acids) and even some metals 

  • Antigens do not need to be attached to a pathogen or cell --> they can simply be free-floating molecules. T


2
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  • Self-antigens

  • In vertebrates (an animal of a large group distinguished by the possession of a backbone or spinal column), what are the most important self-markers? —> what two classes can they be divided into + what’s the difference between these two classes


Self-antigens, which are located on the surface of cells, mark the cells of an organism as ‘self’ so that the immune system doesn’t attack them 

  • In vertebrates (an animal of a large group distinguished by the possession of a backbone or spinal column), the most important self-markers are major histocompatibility complex (MHC) markers (also known as MHC proteins, MHC molecules or self-antigens) which bind antigen fragments (peptides) and present them on the surface of cells, and can be divided into two different classes 

    • MHC Class I markers are expressed on all nucleated cells in the body --> so all cells in the human body except for those without a nucleus (e.g. red blood cells) express MHC Class I markers 

    MHC Class II markers are found on specialised cells of the immune system alongside MHC Class 1 markers --> these are known as antigen presenting cells 


<p><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Self-antigens, which are located on the surface of cells, mark the cells of an organism as ‘self’ so that the immune system doesn’t attack them</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ul><li><p class="Paragraph SCXO209118272 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">In vertebrates (an animal of a large group distinguished by the possession of a backbone or spinal column), the most important self-markers are <strong>major histocompatibility complex (MHC) markers </strong>(also known as MHC proteins, MHC molecules or self-antigens) which bind antigen fragments (peptides) and present them on the surface of cells, and can be divided into two different classes</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ul><li><p class="Paragraph SCXO209118272 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;"><strong>MHC Class I markers</strong> are expressed on all nucleated cells in the body --&gt; so all cells in the human body except for those without a nucleus (e.g. red blood cells) express MHC Class I markers</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p class="Paragraph SCXO209118272 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;"><strong>MHC Class II markers</strong> are found on specialised cells of the immune system alongside MHC Class 1 markers --&gt; these are known as antigen presenting cells</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p></p>
3
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The MHC markers found on our cells differ between individuals


  • Explain how this creates problems during an organ transplant + how could this problem be fixed

  • T or F? Red blood cells have the same self-marking antigens which are glycoproteins on the surface


  • An organ transplant, the MHC Class I markers expressed on the donor organ will be different to the MHC Class I markers of the organ receiver, which can stimulate the receiver’s immune system to recognise the transplanted organ as non-self and launch an attack 

  • Therefore, organ transplant recipients must routinely take immunosuppressants in order to prevent the immune system from attacking the donated organ 

 

  • F. Red blood cells have different self-marking antigens which are glycoproteins on the surface of the cell and give the specific blood types 


4
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  • Non-self antigens + what happens if they are recognised

  • Outline what the plasma membrane of immune cells has


Non-self antigens are antigens that the immune system reads as ‘foreign’/ not belonging to that individual -  If a non-self antigen is recognised within the body, the immune system is activated and attempts to eliminate it 

 

The plasma membrane of immune cells has:  

1. Self-antigens that identify the immune cell as ‘self’ 

2. Receptors for self-antigens so that the immune cell can identify self-cells  

3. Receptors for foreign antigens so that the immune cell can identify non-self-cells and signal other immune cells to destroy it 


<p><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Non-self antigens are antigens that the immune system reads as ‘foreign’/ not belonging to that individual -&nbsp; If a non-self antigen is recognised within the body, the immune system is activated and attempts to eliminate it</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO210696617 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO210696617 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">The plasma membrane of immune cells has:&nbsp;</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO210696617 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">1. Self-antigens that identify the immune cell as ‘self’</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO210696617 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">2. Receptors for self-antigens so that the immune cell can identify self-cells&nbsp;</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO210696617 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">3. Receptors for foreign antigens so that the immune cell can identify non-self-cells and signal other immune cells to destroy it</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO210696617 BCX0" style="text-align: left;"></p>
5
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  • Autoimmune disease

  • How does it occur

  • Examples


  • Disease in which an individual’s immune system initiates an immune response against their own cells

  • A malfunction involving antigens can occur when an error in the immune system results in the recognition of self-antigens as non-self --> resulting in the immune system attacking self-cells

  • Autoimmune diseases include rheumatoid arthritis and lupus


6
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  • Allergen + are they dangerous?

  • Allergic reactions

  • Mild symptoms

  • Severe symptoms


  • a subcategory of non-pathogenic/harmful antigens + no

  • an overreaction to the presence of an allergen which the immune system recognises as non-self and initiates a strong immune response towards

  • Mild symptoms of allergic reactions can include: an itchy rash, runny nose, sneezing, shortness of breath, and swelling

  • However, in more severe cases, constriction of airways, increased permeability of blood vessels, difficulty breathing, and decreased blood pressure may also be observed + death


7
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  • Cellular pathogens + examples

  • Non-cellular pathogens + examples

  • Infection

  • Disease

  • Incubation period


Cellular pathogens have a cellular structure with organelles and are living organisms 

e.g. 

  • Bacteria 

  • Fungi 

  • Protozoa 

  • Parasites 

  • Worms 

 

Non-cellular pathogens do not have a cellular structure and are non-living 

e.g. 

  • Viruses 

  • Prions 

 

  • An infection occurs when pathogens enter the human body and once in the body begin to multiply 

  •  A disease occurs when the body’s cells or organs are damaged by the pathogens/affects the normal functioning of them and signs and symptoms of the disease become obvious 

  • The time after infection and before the first symptoms of a disease appear is called the incubation period 


8
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  • Extracellular threats + can they interfere with the cells’ functioning

  • Intracellular threats


  • Extracellular threats are threats found outside of a cell that can interfere with its functioning (e.g. bacteria) 

  • Intracellular threats are threats found within a cell that can interfere with its functioning (e.g. viruses) 


9
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List examples of cellular pathogens

  • Bacteria

  • Fungi

  • Worms

  • Protozoa


10
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  • Bacteria + are they a pathogen & if so, how can they damage cells/cause disease?

  • How they typically reproduce

  • Structure

  • What toxins do they release


  • Unicellular prokaryotes that can infect almost

    any part of the body. Bacteria can cause disease

    through the production of toxins and enzymes

    which either affect the functioning of cells or cause

    their death.

  • Asexually via binary fission


Structure

  • All bacteria have a cell wall made of peptidoglycan, a cell membrane and a single circular chromosome of DNA 

  • Many bacteria have plasmids (small circular pieces of double stranded DNA) 

 

  • Some bacteria produce toxins that damage host tissues and cause disease 

    - Exotoxins – are highly soluble proteins produced by bacteria as part of their metabolism  

    • released into surroundings as bacteria grow  

    • inhibit protein synthesis 

    • damage cell membranes or disrupt membrane transport 

    • interfere with nerve functions  

    --> Tetanus and cholera are 2 diseases caused by exotoxin producing bacteria 

     

    • Endotoxins – are lipid based and are released when bacteria die 

    • fever, diarrhoea, chills, tissue death may result from endotoxin producing bacteria 

    --> Typhoid fever and meningitis are 2 diseases caused by endotoxin producing bacteria 


11
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  • Fungi

  • Worms

  • Protozoa


Plus how does each reproduce


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12
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List examples of non-cellular pathogens

  • Viruses

  • Prions


13
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Viruses + how they reproduce

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14
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  • Prions

  • Which organisms do they only occur in + which organ/structures do they affect

  • How they reproduce + do they have genetic material

  • T or F? Prion diseases are both rare and always fatal


  • Do not contain genetic material 


Prion protein can exist in 2 forms  

1. a normal form of protein called PrPC produced by cells normally, usually in the central nervous system 

2. a harmful infectious form of protein called PrPSc  

--> difference between the normal and harmful forms is due to the secondary structure of the protein 

 

Reproduction

  • Whenever a prion comes in contact with a normal prion protein, it somehow causes the normal protein to ‘flip’ into a twisted shape, thereby becoming a prion (abnormal protein) Any other normal protein that a twisted prion touches will also be converted, producing a chain reaction 

 

  • Prion proteins are insoluble, infectious even at high temperatures, and are almost indestructible (thus, they cannot be fully broken down by proteases) 


  • True. Prion diseases are rare but always fatal 


<ul><li><p class="Paragraph SCXO233067901 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Do not contain genetic material</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p class="Paragraph SCXO233067901 BCX0" style="text-align: left;"></p><p class="Paragraph SCXO233067901 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Prion protein can exist in 2 forms&nbsp;</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO233067901 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">1. a normal form of protein called PrPC produced by cells normally, usually in the central nervous system</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO233067901 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">2. a harmful infectious form of protein called PrPSc&nbsp;</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO233067901 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">--&gt; difference between the normal and harmful forms is due to the <u>secondary structure</u> of the protein</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO233067901 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO233067901 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">Reproduction</span></p><ul><li><p class="Paragraph SCXO233067901 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Whenever a prion comes in contact with a normal prion protein, it somehow causes the normal protein to ‘flip’ into a twisted shape, thereby becoming a prion (abnormal protein) Any other normal protein that a twisted prion touches will also be converted, producing a chain reaction</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p class="Paragraph SCXO233067901 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ul><li><p class="Paragraph SCXO233067901 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Prion proteins are insoluble, infectious even at high temperatures, and are almost indestructible (thus, they cannot be fully broken down by proteases)</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p class="Paragraph SCXO233067901 BCX0" style="text-align: left;"></p><ul><li><p class="Paragraph SCXO233067901 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">True. Prion diseases are rare but always fatal</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p></p>
15
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  • Innate immune system/non-specific immune system

  • What is it composed of?

  • Non-specific response meaning

  • T or F? This system responds to injury and antigens extremely slowly


Innate immune system/non-specific immune system: a component of the immune system that is composed of generalised and non-specific defences and/or responses to pathogens 

  • It is composed of two different defences known as the first and second lines of defences 

 

--> Both of these mechanisms involve a non-specific response to foreign antigens, responding the same way regardless of the type of pathogen or antigen present 

 

False. Another characteristic of these two mechanisms is that they respond to injury and antigens extremely quickly – within minutes to hours they already begin to limit the spread of infection and stimulate local changes at the site of injury 

16
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  • First line of defence


First line of defence: a component of the innate immune system characterised by the presence of physical, chemical, and microbiological barriers to keep pathogens out of the host organism

17
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What are the two types of barriers present in the first line of defence of plants + describe them but don’t give examples

There are two types of barriers present in the first line of defence of plants – physical and chemical barriers 

  • Physical barrier feature solid or fluid obstacles that block pathogen entry such as skin or mucus 

  • Chemical barrier feature the use of  chemicals such as enzymes, toxins, and acids to protect against pathogen invasion/protect against spread of disease (e.g. by destroying or slowing their growth) 


18
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Examples of barriers in plants (both physical and chemical)

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What is a barrier that animals have that plants do not. Explain it and how it acts as a barrier.

  • While animals have physical and chemical barriers, they also have microbiological barriers -  a component of the first line of defence in which the presence of normal flora (normal, harmless microorganisms) limits the growth of pathogenic bacteria 

 

They can do this by: 

  • They compete for space. If beneficial bacteria are already covering a surface (such as your skin or intestines), there is less room for harmful bacteria to settle.  

  • They compete for nutrients. They use up the available food, making it harder for pathogens to survive.  

  • They produce substances that inhibit pathogens. Some normal bacteria release acids or antimicrobial chemicals that slow or kill harmful microbes.  

  • They help stimulate the immune system. Their presence helps your immune system stay prepared to respond to infections. 


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Why is the respiratory tract, gastrointestinal tract, and genitourinary tract, despite being inside the body, are in the first line of defence

  • They are still considered exposed to the outside environment because they have openings to the outside (such as the nose, mouth, and urethra) 

  • Because the pathogens are stopped before they enter the body's tissues, these are all part of the first line of defence. 

  • The second line of defence only begins if pathogens cross these barriers and invade the body's tissues or bloodstream


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Examples of barriers in animals

Physical 

Barriers that prevent or impede entry of pathogens 

Intact skin and body surfaces 

This means that unbroken skin and the linings of certain body systems act as barriers to keep pathogens out. 

Examples include: 

  • Integumentary tract = skin  

    • Acts like a protective wall that germs cannot easily pass through 

     

  • Respiratory tract = airways and lungs  

    • Lined with mucus and tiny hairs to trap germs.  

 

  • Gastrointestinal tract = digestive system  

    • Helps destroy germs with stomach acid and digestive enzymes 

     

  • Genitourinary tract = urinary and reproductive systems  

    • Urine flow and mucus help flush away microbes 

 

  • 🛡 Skin → blocks germs from entering.  

  • 👃 Nasal hairs → trap particles.  

  • 🤧 Mucus → traps organisms.  

  • 🌬 Cilia → sweep mucus and germs to the throat where it is swallowed or coughed out 

  • 🍽 Stomach acid → destroys swallowed pathogens.  

Memory tip: Think "Trap → Sweep → Swallow → Destroy." 

 

  • mechanical flushing activity of urine and intestinal contents 

Chemical 

Barriers that act to inhibit the growth or development of pathogens and/or act to destroy pathogens 

  • Presence of lysozyme enzymes in tears and saliva that destroy bacterial cell walls  

 

  • Acidic sweat that destroys pathogens growing on the surface of the body  

 

  • Stomach acid that destroys pathogens that have been eaten/swallowed  

 

  • Antibacterial compounds in earwax 

 

  • Antibacterial proteins in semen  

 

  • Low pH in the vagina 

 

  • Antibiotics in earwax 

Microbiological 

The presence of non-pathogenic bacteria (known as normal flora) in the body can prevent the growth or colonisation of pathogenic microorganisms as they compete for space and resources 

  • Presence of bacteria on the skin, in the lower gastrointestinal tract, and the vagina 


22
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  • Second line of defence

  • What are the two components of this line

  • All of the cells involved are called _____


Second line of defence a component of the innate immune system characterised by the non-specific and immediate response to injury that make it past the 1st line of barriers and pathogens by a variety of cells and molecules  

 

There are two components of the second line of defence: cellular and non-cellular components 


All of the cells involved are called leukocytes/white blood cells 

23
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  • Phagocytes

  • Examples of phagocytes (these are important later on) + which of these are antigen-presenting cells? And hence what does this mean? (Hint: MHC markers)


  • A group of leukocytes that engage in phagocytosis, a process in which they consume and destroy pathogens, foreign or dead material present in the body by engulfing it through the process of endocytosis

  • Phagocytes include neutrophils, macrophages (immature = monocytes), and dendritic cells 

—> macrophages and dendritic cells – are also known as antigen-presenting cells/professional antigen-presenting cells  where they do not only consume and destroy foreign material, but they also present antigens from consumed material on their surface using MHC Class II 


Think of Neutrophils as - NA - Neutrophils & antigen-presenting cells - “NAH they’re not an APC”


<ul><li><p><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">A group of leukocytes that engage in phagocytosis, a process in which they consume and destroy pathogens, foreign or dead material present in the body by engulfing it through the process of endocytosis</span></p></li><li><p><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Phagocytes include neutrophils, macrophages (immature = monocytes), and dendritic cells</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">—&gt; macrophages and dendritic cells – are also known as antigen-presenting cells/professional antigen-presenting cells&nbsp;</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">where they do not only consume and destroy foreign material, but they also present antigens from consumed material on their surface using MHC Class II</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p></p><p><span style="line-height: 20.7px; color: windowtext;">Think of Neutrophils as - NA - Neutrophils &amp; antigen-presenting cells - “NAH they’re not an APC”</span></p><p></p>
24
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Diagram of phagocytosis

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  • Cytokines


To communicate within the immune system, phagocytes release a number of substances such as cytokines – which are important cell signalling molecules which help protect against pathogens and can help guide immune cells to the site of infection or injury 

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  • Natural killer cells

  • How do they kill damaged/infected cells?


A type of leukocyte responsible for the recognition and destruction of damaged and/or infected host cells 

  • This is achieved with the presence of two receptors – a killer inhibitory receptor and a killer activation receptor 

    • Killer inhibitory receptor – examines the surface of cells for MHC Class I markers 

    • Killer activation receptor – binds to certain molecules which appear on cells undergoing cellular stress (e.g. infected or cancerous cells) 

 

The presence of MHC Class I markers can be altered due to a number of different disease processes  

e.g. 

  • MHC Class I markers may be absent due to the presence of a viral infection, which can either destroy or suppress the production of MHC Class I markers 

  • Also the gene expression of MHC Class I markers may be affected in cancer cells, also leading to the absence of MHC Class I markers 

 

  • If the killer inhibitory receptor detects a sufficient number of MHC Class I markers, then it overrides/disallow the killer activation signal, preventing cell death 

  • Whereas, when the killer activation receptor is activated and the killer inhibitory receptor is unable to bind to a sufficient number of MHC Class I markers in infected or abnormal cells --> Cell death is initiated 

 

<p><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">A type of leukocyte responsible for the recognition and destruction of damaged and/or infected host cells</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ul><li><p class="Paragraph SCXO191002577 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">This is achieved with the presence of two receptors – a killer inhibitory receptor and a killer activation receptor</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ul><li><p class="Paragraph SCXO191002577 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Killer inhibitory receptor – examines the surface of cells for MHC Class I markers</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li><li><p class="Paragraph SCXO191002577 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Killer activation receptor – binds to certain molecules which appear on cells undergoing cellular stress (e.g. infected or cancerous cells)</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul></li></ul><p class="Paragraph SCXO191002577 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO191002577 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">The presence of MHC Class I markers can be altered due to a number of different disease processes&nbsp;</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO191002577 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">e.g.</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ul><li><p class="Paragraph SCXO191002577 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">MHC Class I markers may be absent due to the presence of a viral infection, which can either destroy or suppress the production of MHC Class I markers</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li><li><p class="Paragraph SCXO191002577 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Also the gene expression of MHC Class I markers may be affected in cancer cells, also leading to the absence of MHC Class I markers</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p class="Paragraph SCXO191002577 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ul><li><p class="Paragraph SCXO191002577 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">If the killer inhibitory receptor detects a sufficient number of MHC Class I markers, then it overrides/disallow the killer activation signal, preventing cell death</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li><li><p class="Paragraph SCXO191002577 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Whereas, when the killer activation receptor is activated and the killer inhibitory receptor is unable to bind to a sufficient number of MHC Class I markers&nbsp;in infected or abnormal cells --&gt; Cell death is initiated</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p class="Paragraph SCXO191002577 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p>
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  • Mast cells + where do they reside

  • Eosinophils + which pathogens do they typically target


Mast cells 

A type of leukocyte that detects injury to surrounding cells or are stimulated by antigens or allergens, where they become activated and degranulate, releasing histamine during allergic and inflammatory responses 

  • They reside in connective tissues throughout the body 

 

Eosinophils 

A large granular leukocyte responsible for the release of toxic proteins such as DNases, RNases, and proteases which help destroy invading pathogens 

  • They typically target pathogens which are too large to be phagocytosed 


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  • Are interferon and complement proteins cellular or non-cellular components of the second line of defence

  • Interferon


  • Non-cellular

Interferon  - A cytokine released by virally infected cells which interact with receptors on neighbouring uninfected cells, causing them to undergo a number of changes that make them less susceptible/more resistant to viral infection --> this helps prevent the virus from spreading between cells 

• produced by almost all cells of the immune system, but especially T cells


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  • Complement proteins

  • Complement cascade


Complement proteins  

A number of different types of proteins found in the blood that opsonise, cause lysis, and attract phagocytes to invading pathogens 

  • In the presence of certain pathogens, these proteins begin reacting with each other in a series of reactions called the complement cascade 


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Describe the outcomes of the complement cascade 

Memory trick (maybe)

Put a SIGN ON it - Opsonisation —> "Eat Me!" sticker

Chemical Taxi - Chemotaxis —> taxis following a GPS signal

<p>Memory trick (maybe)</p><p>Put a SIGN ON it - Opsonisation —&gt; "Eat Me!" <u>sticker</u></p><p>Chemical Taxi - Chemotaxis —&gt;  taxis following a GPS signal</p>
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  • Fever

  • Why does it occur + is it a specific response?

  • Do prolonged fevers have detrimental impacts?


Fever 

A temporary increase in body temperature 

  • A complex series of responses can raise the set temperature point of the body during a fever   --> In response, the body initiates a number of countermeasures that increase core body temperature to reach this new setpoint, including shivering and heat-conserving behaviours (e.g. putting on a jumper) 

= This an innate response to potential infection, as many pathogens cannot survive at the elevated temperatures created by a fever + fevers help the immune system by activating certain proteins in the body that make them work more efficiently 

 

  • However, it is important to note that prolonged fevers can be detrimental to the body due to your own cells also have difficulty functioning, proteins and enzymes work best around normal body temperature, prolonged high temperatures put stress on the body's tissues


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  • What is the inflammatory response + symptoms

  • Is it specific?

  • List the three main aspects of the inflammatory response


The process of inflammation increases blood flow to an injured area, bringing a greater number of immune cells and components to help clear debris and fight pathogens that may have entered the body

--> this increase in blood and fluid to the affected tissue causes swelling, pain, heat, and redness 

  • It is a complex, non-specific process that always occurs in the same way regardless of the pathogen present or the injury that has occurred 

 

There are three main aspects of the inflammatory response – initiation, vasodilation, and migration 

🧠 “Inflammation Visits Me”

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Go over the three stages of the inflammatory response

Initiation – damage/infection occurs 

Infection occurs which causes the damaging of cells and introduces pathogens such as bacteria into the body 

  • Macrophages (a phagocyte) situated in the tissue become activated and, along with damaged cells, release cytokines +  mast cells degranulate, releasing histamine


Vasodilation

The histamine released from mast cells travels to nearby blood vessels and binds to specific receptors, causing vasodilation which causes increased diameter and permeability of blood vessels, increasing blood flow to the injury site --> this is the reason behind the swelling, redness, pain and warmth


Migration 

The vasodilation allow for a number of innate immune system components to leave the bloodstream and enter the site of injury 

 

This includes: 

  • Phagocytes, including macrophages and neutrophils, leave the blood  and enter the tissue due to increased permeability of blood vessels, where they are guided by the cytokines secreted by activated macrophages and damaged cells to the site of injury --> where they phagocytose pathogens and digest them using enzymes such as lysozymes 

 

  • Complement proteins are attracted to pathogens and make it easier for phagocytes to destroy them 


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What is pus + when does the inflammatory response finish

  • Pus contains a large amount of dead immune cells and pathogens

  • The response continues until the site has been cleared of pathogens and debris, and the site of injury has been healed and will eventually return to normal


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  • Third line of defence/adaptive immune system/specific immune response

  • Its features which separate it from the second line of defence


Third line of defence/adaptive immune system/specific immune response a subset of the immune system within vertebrates that is composed of the humoral and cell-mediated responses which create a specific immune response and form immunological memory 

 

The two features of the adaptive immune system which separate it from the second line of defence: 

  • Specificity – the adaptive immune system responds to each distinct pathogen in a unique manner  

  • Immunological memory – the adaptive immune system results in the production of cells that allow the body to respond to future re-infections by a previously encountered pathogen quickly and effectively 


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Describe the process of antigen presentation

  1. After antigen-presenting cells (APCs) engulf and digest pathogens via phagocytosis, displaying pathogenic antigens on their MHC Class II markers --> they then travel via the lymphatic system to lymph nodes 

 

  1. T-Helper cell with complementary receptor on its surface binds to foreign antibody and is ‘selected’ 

 

  1. The T helper cell then becomes activated/selected 

    --> The activated T helper cell can then help initiate the adaptive immune response through either the humoral or cell-mediated immune responses 


<ol><li><p class="Paragraph SCXO177027049 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">After antigen-presenting cells (APCs) engulf and digest pathogens via phagocytosis, displaying pathogenic antigens on their MHC Class II markers --&gt; they then travel via the lymphatic system to lymph nodes</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ol><p class="Paragraph SCXO177027049 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ol start="2"><li><p class="Paragraph SCXO177027049 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">T-Helper cell with complementary receptor on its surface binds to foreign antibody and is ‘selected’</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ol><p class="Paragraph SCXO177027049 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ol start="3"><li><p class="Paragraph SCXO177027049 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">The T helper cell then becomes activated/selected</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO177027049 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">--&gt; The activated T helper cell can then help initiate the adaptive immune response through either the humoral or cell-mediated immune responses</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ol><p></p>
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  • Humoral immunity (do not describe its response)

  • B lymphocytes


An adaptive immune response in which extracellular pathogens are neutralized or destroyed by the production and secretion of antibodies produced by plasma cells 

  • You can think of it as ‘eh’ —> extracellular - humoral

 

B lymphocytes are a type of white blood cell whose surfaces are covered with B cell receptors (known as membrane-bound antibodies) --> these cells circulate throughout the body in the bloodstream and are found in high numbers within lymph nodes 

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Describe the humoral immune response  + Clonal selection theory

  1. A pathogen with an antigen that is complementary in shape to the antigen-binding site on a B cell receptor binds to the receptor on the B cell --> when this occurs, the B cell is said to have been ‘selected’ 

 

  1. Selected B cell and T-helper cell with a matching receptor to the antigen on the pathogen interact and secrete cytokines --> these cytokines cause the B cell to undergo clonal expansion where many copies of the selected B cell are produced 

 

  1. The T helper cell also stimulates the selected B cell via cytokines to undergo the process of differentiation, in which the clones of the selected B cell differentiate into two different types of B cells: B memory cells and plasma cells 

 

  1. The plasma cells secrete antibodies into the bloodstream in order to destroy selected pathogen


Clonal selection theory: the process in which B and T cells encounter an antigen that matches their antigen binding site, and then generate many copies of themselves 


<ol><li><p class="Paragraph SCXO267728122 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px;">A pathogen with an antigen that is complementary in shape to the antigen-binding site on a B cell receptor binds to the receptor on the B cell --&gt; when this occurs, the B cell is said to have been ‘selected’</span><span style="line-height: 20.7px;">&nbsp;</span></p></li></ol><p class="Paragraph SCXO267728122 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ol start="2"><li><p class="Paragraph SCXO267728122 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Selected B cell and T-helper cell with a matching receptor to the antigen on the pathogen interact and secrete cytokines --&gt; these cytokines cause the B cell to undergo clonal expansion where many copies of the selected B cell are produced</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ol><p class="Paragraph SCXO267728122 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ol start="3"><li><p class="Paragraph SCXO267728122 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">The T helper cell also stimulates the selected B cell via cytokines to undergo the process of differentiation, in which the clones of the selected B cell differentiate into two different types of B cells: B memory cells and plasma cells</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ol><p class="Paragraph SCXO267728122 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ol start="4"><li><p class="Paragraph SCXO267728122 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">The plasma cells secrete antibodies into the bloodstream in order to destroy selected pathogen</span></p></li></ol><p class="Paragraph SCXO267728122 BCX0" style="text-align: left;"></p><p class="Paragraph SCXO267728122 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;"><strong>Clonal selection theory: </strong>the process in which B and T cells encounter an antigen that matches their antigen binding site, and then generate many copies of themselves</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p></p>
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What are B memory cells responsible for?

A differentiated B lymphocyte that reside in the body for a prolonged period of time and are responsible for providing long-lasting immunological memory of an antigen 

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Antibodies/immunoglobulins:

  • The type of molecule they are + what structure of that molecule

  • Describe its structure

  • T or F? There are different classes of antibodies - the type of light chain determines the class to which the antibody belongs

  • How many antigen binding sites present?

  • Sketch a labelled diagram


  • Antibodies released by plasma cells are proteins with a quaternary structure


Structure

--> They are composed of four polypeptide chains, including two heavy chains and two light chains, arranged into a ‘Y’ shape 

  • The two heavy chains are joined by a disulphide bond - a strong covalent bond occurring between two sulphur atoms  

  • Each antibody has two regions --> the ‘stem’ of the antibody is known as the constant region which does not vary, and the tops of the ‘arms’ are known as the variable region that differ between antibodies 


  • False. There are different classes of antibodies - the type of heavy chain determines the class to which the antibody belongs 


  • There are two antigen binding sites present --> hence an antibody can bind with two pathogens at once 


<ul><li><p class="Paragraph SCXO224191062 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Antibodies released by plasma cells are proteins with a <u>quaternary structure</u></span></p></li></ul><p class="Paragraph SCXO224191062 BCX0" style="text-align: left;"></p><p class="Paragraph SCXO224191062 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Structure</span></p><p class="Paragraph SCXO224191062 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;"> --&gt; They are composed of four polypeptide chains, including two heavy chains and two light chains, arranged into a ‘Y’ shape</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ul><li><p class="Paragraph SCXO224191062 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">The two heavy chains are joined by a disulphide bond - a strong covalent bond occurring between two sulphur atoms&nbsp;</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li><li><p class="Paragraph SCXO224191062 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Each antibody has two regions --&gt; the ‘stem’ of the antibody is known as the constant region which does not vary, and the tops of the ‘arms’ are known as the variable region that differ between antibodies</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p class="Paragraph SCXO224191062 BCX0" style="text-align: left;"></p><ul><li><p class="Paragraph SCXO224191062 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">False. There are different classes of antibodies - the type of <u>heavy </u>chain determines the class to which the antibody belongs</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p class="Paragraph SCXO224191062 BCX0" style="text-align: left;"></p><ul><li><p class="Paragraph SCXO224191062 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">There are two antigen binding sites present --&gt; hence an antibody can bind with two pathogens at once</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p></p>
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  • What are the standard five types of antibodies

  • Are antibodies specific?


There are five types of antibodies – IgA, IgD, IgE, IgG, IgM --> which are all secreted at different times in the immune response

"A Doctor Eats Green Marshmallows."

  • A = IgA

  • Doctor = IgD

  • Eats = IgE

  • Green = IgG

  • Marshmallows = IgM

Due to the process of clonal selection, these antibodies are specific and have an antigen-binding site that is complementary to the antigens located on the pathogen

<p><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">There are five types of antibodies – IgA, IgD, IgE, IgG, IgM --&gt; which are all secreted at different times in the immune response</span></p><p><strong>"A Doctor Eats Green Marshmallows."</strong></p><ul><li><p><strong>A</strong> = <strong>IgA</strong></p></li><li><p><strong>Doctor</strong> = <strong>IgD</strong></p></li><li><p><strong>Eats</strong> = <strong>IgE</strong></p></li><li><p><strong>Green</strong> = <strong>IgG</strong></p></li><li><p><strong>Marshmallows</strong> = <strong>IgM</strong></p></li></ul><p><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Due to the process of clonal selection, these antibodies are specific and have an antigen-binding site that is complementary to the antigens located on the pathogen</span></p>
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Describe the different ways antibodies interact with pathogenic antigens in a number of key ways in the humoral immune response

knowt flashcard image
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  • Cell-mediated immunity (don’t explain its response)

  • Cytotoxic T cells


Cell-mediated immunity 

Infected or abnormal cells are destroyed by cytotoxic T-cells (T cell immunity). This relates to intracellular threats where the virus has entered the cell  

 

Cytotoxic T cells, a type of T lymphocyte, primarily carry out their role by assessing the MHC Class I marker of infected cells (nucleated cells) 

  • Where in addition to their role of self-recognition, MHC Class I can also display foreign antigens that have been broken down in a cell on its surface 


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Describe cell-mediated immune response  

  1. T-helper cell releases cytokines + APC MHC class I markers that present complementary antigens to receptors on naive Cytotoxic T cell —> stimulates/activates naïve Cytotoxic-T cell  = selected

 

  1. The selected cytotoxic T cell to undergo clonal expansion and differentiation 

 

  1. The clones of the selected T cell differentiate into two types of T cells – effector cells called cytotoxic T cells, and T memory cells 

    • T memory cells reside in the body for extended periods of time and help form immunological memory 

    • The majority of selected T cells differentiate into cytotoxic T cells, which leave the lymph node and travel throughout the body, reaching the site of infection 


  1. Once the cytotoxic T cell has found an abnormal cell that is presenting complementary foreign antigens on its MHC Class I complex, it binds to it  

 

  1. Chemicals, such as perforin, are then secreted by the cytotoxic T cell to induce apoptosis in the infected or abnormal cell  


<ol start="5"><li><p class="Paragraph SCXO93325056 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">T-helper cell releases cytokines + APC MHC class I markers that present complementary antigens to receptors on naive Cytotoxic T cell —&gt; stimulates/activates naïve Cytotoxic-T cell&nbsp;</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;= selected</span></p></li></ol><p class="Paragraph SCXO93325056 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ol start="6"><li><p class="Paragraph SCXO93325056 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">The selected cytotoxic T cell to undergo clonal expansion and differentiation</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ol><p class="Paragraph SCXO93325056 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ol start="7"><li><p class="Paragraph SCXO93325056 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">The clones of the selected T cell differentiate into two types of T cells – effector cells called cytotoxic T cells, and T memory cells</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ul><li><p class="Paragraph SCXO93325056 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">T memory cells reside in the body for extended periods of time and help form immunological memory</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li><li><p class="Paragraph SCXO93325056 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">The majority of selected T cells differentiate into cytotoxic T cells, which leave the lymph node and travel throughout the body, reaching the site of infection</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul></li></ol><p class="Paragraph SCXO93325056 BCX0" style="text-align: left;"></p><ol start="8"><li><p class="Paragraph SCXO93325056 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Once the cytotoxic T cell has found an abnormal cell that is presenting complementary foreign antigens on its MHC Class I complex, it binds to it&nbsp;</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ol><p class="Paragraph SCXO93325056 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ol start="9"><li><p class="Paragraph SCXO93325056 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Chemicals, such as perforin, are then secreted by the cytotoxic T cell to induce apoptosis in the infected or abnormal cell&nbsp;</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ol><p></p>
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Compare humoral and cell-mediated response 

 

Antibody-mediated (Humoral) response  

Cell-mediated response  

Similarities 

Both involved T helper cells -both are specific -both involve recognition of presented antigens

Involve WBC that reside in lymph nodes  

 

Differences 

-occurs in blood, lymph and tissue fluids  

  • Pathogens destroyed

-involves B cells and antibodies 

-infected cells  

-doesn’t involve B cells/antibodies 


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  • Immunological memory 

  • Explain how B and T memory cells respond to the same pathogen entering


The ability of the immune system to quickly and aggressively combat a previously encountered pathogen due to the presence of T and B memory cells  


If the same pathogen enters again: 

  • The B memory cells recognise the antigen straight away because they have receptors that match it 

  • They rapidly divide (clonal expansion) into new antibody-producing plasma cells  

  • The plasma cells produce large amounts of antibodies much faster than during the first infection 


(B memory cells also create immunological memory by constantly secreting low amounts of their antibody)

 

When the same pathogen enters again: 

  • An antigen-presenting cell (APC) displays the familiar antigen.  

  • The T memory cells recognise it immediately.  

  • They rapidly divide into: 

    • T helper cells (which release cytokines)  

    • Cytotoxic T cells (which kill infected cells) 


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Sketch a labelled diagram comparing the processes of humoral and cell-mediated immunity:

knowt flashcard image
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  • Functions of the lymphatic system 

  • What is the lymphatic system comprised of


  • Act as a transport network for the antigen presenting cells – location of clonal selection and expansion 

  • Production of leukocytes/WBC, including lymphocytes in primary lymphoid tissues 

  • Removal of fluid from tissues around the body  

  • Absorption of fatty acids from the digestive system 


The lymphatic system is comprised of a series of lymphatic vessels throughout the body that function to transport lymph to a number of primary and secondary lymphoid tissues 


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  • Primary lymphoid tissues 

  • What are the main primary lymphoid tissues + their function


Primary lymphoid tissues 

Components of the lymphatic system that are responsible for the production and maturation of lymphocytes 

  • Where the main primary lymphoid tissues include the bone marrow and the thymus  

    • The production of B and T lymphocytes occurs in the bone marrow, which is primarily found inside long bones such as the femur and humerus --> while B lymphocytes remain in the bone marrow to mature further (think of it as B cells = bone marrow), T lymphocytes travel to the thymus to mature (think of it as T cells = thymus)


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  • secondary lymphoid tissues 

  • What are the main secondary lymphoid tissues + their function

  • Why do lymph nodes swell when one is sick


Secondary lymphoid tissues 

Components of the lymphatic system that are responsible for the maintenance of mature lymphocytes and the activation of the adaptive immune response 

  • The main secondary lymphoid tissues include the lymph nodes (that act as filters), tonsils and the spleen 

  • In these tissues, mature lymphocytes are clustered together and ‘scan’ passing lymph for the presence of any pathogens or foreign antibodies on antigen-presenting cells 


--> If a foreign antigen matches the receptors of specific lymphocytes, these lymphocytes then undergo clonal selection and differentiation which results in a large number of B and T cells being created within these tissues --> resulting in the characteristic swelling of lymph nodes when you’re sick 

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Lymphatic drainage 

  • Lymphatic capillaries + what do they collect

  • Lymph


Lymphatic capillaries are extremely small vessels that exist throughout the tissues of the body 

They collect: 

  • Excess tissue fluid  

  • Proteins  

  • Dead cells  

  • Pathogens 

  • Immune cells, including antigen-presenting cells (APCs) 

     

Once the clear fluid enters these capillaries – it is called lymph where it is carried away into the lymphatic system, where it eventually arrives at a lymph node 

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Lymphatic flow 

The small lymphatic capillaries throughout the body gradually join together to form larger vessels that contain an increasing amount of lymph

  • Describe what type of walls these vessels have and how squeeze lymph fluid through the system

  • T or F? These vessels are one-way valves.


  • These vessels have thin walls and rely on surrounding muscle movements to squeeze lymph fluid through the system (note: the heart is not responsible for pumping lymph) 

  • True. These vessels feature a number of one-way valves --> so fluid moves in one direction only – away from the tissues and towards the lymph nodes 


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Lymphatic surveillance 

  1. The fluid drained from tissues arrives at lymph nodes via afferent lymphatic vessels – where the lymph travels through clusters of B and T cells 

--> As it drains through these clusters, antigen-presenting cells and pathogens are most likely to meet a lymphocyte with a matching antigen receptor which stimulates the process of clonal selection + expansion 


  • What happens once an adaptive immune response is initiated? (hint: antibodies & activated cytotoxic T cells)

  • T or F? This lymph is then returned into circulation near the heart, where the lymphatic vessels join with the large veins returning blood back to the heart

  • Is the adaptive immune system slower to activate than the innate immune system?


  • If an adaptive immune response is initiated, antibodies and activated cytotoxic T cells will be transported in the lymph away from the lymph nodes via efferent lymphatic vessels 


  • T


  • Unlike the innate immune system, which provides an immediate source of protection, the adaptive immune system is much slower to activate 


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  • Immunity

  • Natural immunity

  • Artificial immunity/induced immunity

  • Active immunity

  • Passive immunity + is it long-term?


Immunity is resistance to particular infectious disease or pathogen 

 

Natural immunity protection against a disease formed without medical intervention 

Artificial immunity/induced immunity protection against a disease formed as a result of medical intervention 

 

A person's immunity to a disease is further classified based on the strategy used to develop it: 

  • Active immunity protection against a disease created by antibodies and memory cells formed by a person’s own adaptive immune system 

  • Passive immunity protection against a disease created by antibodies from an external source 

--> Passive immunity is temporary and there is no memory involved 


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Natural active immunity

Natural active immunity  protection against a disease created by antibodies and memory cells produced by an individual’s own immune system without medical intervention 

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  • Natural passive immunity

  • Methods of acquiring natural passive immunity include:


Natural passive immunity protection against a disease created by antibodies from a natural external non-medical source 

 

Two methods of acquiring natural passive immunity include: 

  • Breastfeeding – human breast milk contains many nutrients and proteins essential for healthy growth and development, including antibodies generated from the mother’s own immune system --> once ingested, these antibodies are absorbed into the baby’s bloodstream and protect them against pathogens  

  • Placenta – during pregnancy, some antibodies produced by the mother are able to cross the placenta and enter the foetus’ bloodstream via the umbilical cord 

 

These are important, as babies have poorly developed adaptive immune systems and aren’t able to fully protect themselves against pathogens for the first few months of life – however the duration of protection is shorter as antibodies are quickly degraded 

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  • Artificial active immunity

  • Outline a way to achieve artificial active immunity


Artificial active immunity protection against a disease created by antibodies and memory cells produced by an individual’s own immune system after medical intervention 

 

A way of achieving artificial active immunity is vaccines

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Explain how vaccines help achieve artificial active immunity (don’t talk about the two main phases yet)

  • Vaccines are medical treatments that contain components that resemble a certain pathogen’s antigens, but these components are not able to cause disease 

These components can be: 

  • Attenuated (weakened) or inactivated (dead) pathogens 

  • Toxoids (toxins that have been altered so they can’t cause disease) 

  • Specific proteins from the surface of pathogens 

  • RNA that enters immune cells and causes them to make pathogen-like proteins 

 

  • A person’s adaptive immune system recognises these components as foreign and develops a response to them --> this means that when this individual encounters the actual pathogen in the future, their immune system has antibodies and memory B cells that can target its antigens and rapidly attack it 


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There are two main phases to forming artificial active immunity in vaccines – the primary immune response and the secondary immune response.

Explain both and draw a diagram:

  1. After a person receives their first vaccination, there is a delay in the adaptive immune system’s response because the adaptive immune response is relatively slow --> it takes time for antigen-presenting cells to find T and B cells complementary to the vaccine’s antigen and for the process of clonal selection to occur 

Once the primary immune response had taken place - a moderate number of antibodies and memory cells are formed 

 

  1. Upon receiving a second vaccination, the memory cells created by the first vaccine quickly recognise the antigen in the vaccine and mount a rapid, large secondary immune response --> resulting in the generation of a large number of antibodies and memory cells that go on to create long-lasting immunity



<ol><li><p class="Paragraph SCXO171764792 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">After a person receives their first vaccination, there is a delay in the adaptive immune system’s response because the adaptive immune response is relatively slow --&gt; it takes time for antigen-presenting cells to find T and B cells complementary to the vaccine’s antigen and for the process of clonal selection to occur</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ol><p class="Paragraph SCXO171764792 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Once the primary immune response had taken place - a moderate number of antibodies and memory cells are formed</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><p class="Paragraph SCXO171764792 BCX0" style="text-align: left;"><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ol start="2"><li><p class="Paragraph SCXO171764792 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Upon receiving a second vaccination, the memory cells created by the first vaccine quickly recognise the antigen in the vaccine and mount a rapid, large secondary immune response --&gt; resulting in the generation of a large number of antibodies and memory cells that go on to create long-lasting immunity</span></p></li></ol><p class="Paragraph SCXO171764792 BCX0" style="text-align: left;"></p><p></p>
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Note that more than one vaccination typically needs to take place in order for immunity to be formed

  • T or F? With subsequent immune responses each generating smaller, less rapid responses until long-lasting immunity has been achieved

  • What ways can vaccines be administered?


  • False. With subsequent immune responses each generating larger, more rapid responses until long-lasting immunity has been achieved 

  • Vaccines can be administered via an injection or orally in the form of a liquid 


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Explain what booster vaccines are and why are they used?

  • It is normal for memory T and B cells to die after a long period of time --> this means that in individuals who were immunised against a disease many years ago, their immunity may start to decline and they may become susceptible to a disease they were previously immune to 


  • In these individuals, a booster vaccine/shot is administered,  which is simply another injection of the vaccine they received earlier -->  By doing so, any remaining memory cells are stimulated to activate an immune response, generating more antibodies and memory cells to restore their immunity 


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  • Artificial passive immunity

  • How is it typically achieved


Artificial passive immunity protection against a disease created by antibodies from an external medical source 

  • This occurs through an injection or an infusion (e.g. antiserum for a snake bite) 


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Explain why passive immunity is not long-term:

  • Antibody treatments immediately increase the number of antibodies in the blood, but over time these antibodies degrade until they’ve all disappeared and the immunity they created has gone 

  • As if someone is only given antibodies, they will not develop active immunity because the antibodies they receive will not trigger production of the memory cells responsible for immunological memory 


<ul><li><p class="Paragraph SCXO263631721 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Antibody treatments immediately increase the number of antibodies in the blood, but over time these antibodies degrade until they’ve all disappeared and the immunity they created has gone</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li><li><p class="Paragraph SCXO263631721 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">As if someone is only given antibodies, they will not develop active immunity because the antibodies they receive will not trigger production of the memory cells responsible for immunological memory</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p></p>
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  • Herd immunity 

  • How is it achieved

  • It is particularly crucial for protecting people who?

  • And how does it protect those people?


Herd immunity 

Protection against a disease given to non-immune individuals when a high percentage of a population/herd is immune to the same disease 

  • It is often achieved through high rates of vaccination 

  • It is particularly crucial for protecting people who cannot be vaccinated --> including children who are too young to be vaccinated, people with immune system problems, and those who are too ill to receive vaccines (such as some cancer patients) 


This occurs as: 

  • When a sufficiently large proportion of people in a population are immune to a disease via vaccination --> then the pathogen causing that disease cannot easily reproduce and spread throughout 

  • This then protects the people who aren’t immune as they are now highly unlikely to come into contact with a person harbouring the pathogen and therefore won’t become sick 


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  • Non-infectious diseases

  • Infectious diseases

  • Contagious diseases


Non-infectious diseases aren’t caused by pathogens 

There are many causes of non-infectious diseases 

  • Some non-infectious diseases, such as cystic fibrosis, are caused by abnormal genes 

  • While others, like cardiovascular disease, are largely caused by lifestyle factors such as diet and exercise 

 

Infectious diseases are diseases caused by pathogens 

  • These pathogens harm their host, and cause the symptoms that patients present with 


  •  A subset of infectious diseases are contagious diseases, which are infectious diseases that can be transmitted and spread between different people  


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Contagious vs Virulence 

  • Contagious a property of a pathogen or disease meaning that it can be transmitted from one organism to another  

  • Virulence the potential of a pathogen or disease to cause serious illness or harm 


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  • Emerging diseases

  • Re-emerging diseases


Emerging diseases are diseases that have not occurred in humans before, have occurred previously but only affected particular populations in isolated places, or have occurred throughout history but have only recently been recognised as being caused by pathogens 

 

Re-emerging diseases are diseases that were once major public health problems and then declined dramatically in incidence (frequency in population), but are again becoming health problems for a large number of people 

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Factors contributing to the emergence and re-emergence of diseases 

Factor 

What it means 

Evolution of the causative organism 

Pathogens causing disease can evolve to either infect humans or, if previously capable of infecting humans, evolve to evade treatments by acquiring resistance 

Globalisation and travel 

Due to people being able to quickly travel around the world - an infectious disease that starts in one place can quickly spread around the world 

Increased exposure of humans to animals 

As people expand into forests, farm more land, or climate change changes animal habitats, humans have more contact with animals  

  • Some infectious diseases that are caused by a pathogen transferred from an animal to a human - these are called zoonotic diseases (zoonoses) 

Increasing human population 

More people means more crowded cities and communities. Diseases spread more easily when many people live close together. 

Changing technology 

New technologies or human-made systems can sometimes create environments where pathogens grow and spread 

 

e.g. Legionnaires’ disease is caused by a pathogen that inhabits air conditioning systems 

Insufficient vaccination of the population 

If fewer people are vaccinated, herd immunity decreases --> This means there are more people who can catch and spread the disease, allowing diseases that were once under control to return/spread more easily 


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  • Outbreak 

  • Epidemics

  • Pandemics

  • Endemic 


Outbreak a sudden and unexpected increase in the occurrence of a disease 

 

Disease outbreaks can be classified into one of two categories based on the geographic spread of the disease:  

  • Epidemics involve a sudden, widespread increase in the occurrence of an infectious disease among a specific population in a specific location at a particular time  

 

  • Pandemics involve epidemics that have spread to different countries and/or continents in different regions of the world --> so they typically affect a greater number of people when compared to epidemics and are much more difficult to control 

 

Endemic when a disease occurs at a relatively constant baseline level in a population  

  • So it is always present in a particular population or area at a predictable, relatively constant level --> It doesn't disappear completely, but it also isn't causing unusually large outbreaks all the time 

  • e.g. the flu (influenza) 


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The arrival of the first convicts and settlers from England to Australia in 1788 brought about the introduction of disease and dispossession among the Indigenous population 

Major diseases in Europe during the late 18th century were smallpox, syphilis, tuberculosis, influenza, and measles --> when colonists arrived in Australia, they brought these diseases with them, unleashing them on the local population and causing widespread illness (morbidity) and death (mortality) 


Explain some reasons why these diseases particularly affected the Indigenous population:


Lack of immunity in the Indigenous population 

Many Europeans had caught diseases like measles as children. 

  • They survived the infection.  

  • Their bodies developed natural active immunity, which protected them later in life.  

  • If they caught the disease again, it was usually less severe.  

However for many Indigenous Australians: 

  • It was their first exposure to these diseases.  

  • Many became infected as adults, when diseases such as measles can cause more serious illness.  

  • They had no existing immunity, so diseases spread quickly and caused many deaths. 

 

A lack of knowledge and experience with European diseases 

Before colonisation, Indigenous Australians had extensive knowledge of: 

  • local diseases 

  • traditional medicines 

However, European diseases were completely new. 

This meant they: 

  • did not know how these diseases spread,  

  • did not know effective ways to prevent them,  

  • had no previous experience treating them.  

  • At the same time, many Indigenous communities were prevented from practising their traditional medicine, leaving people with little or no medical care 

 

The disruption caused by colonisation 

Before colonization 

Most Aboriginal and Torres Strait Islander communities: 

  • lived in small, uncrowded, spread-out groups,  

  • had access to clean food and water 

  • had healthy diets (rich in carbs and protein)  —> These conditions generally supported good health. 

After colonization 

European settlement caused major disruptions: 

  • People were removed from their traditional lands.  

  • Access to food and clean water became limited.  

  • Traditional medicine and cultural practices were disrupted.  

  • Many people were forced to live in crowded camps or settlements - made it much easier for infectious diseases to spread. 

Poor nutrition and stress also weakened people's immune systems, making infections more severe. 

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Outline the methods of identifying pathogens

Method 

Explanation 

Example 

Physical 

Uses microscopes to directly observe pathogens - examine their size, shape, arrangement, and structures to help identify them. 

 

Phenotypic 

Identifies pathogens based on their observable characteristics, such as how they grow, their appearance, and their biochemical properties. 

Selective media:  An agar plate designed to allow certain pathogens to grow and multiply to test for their presence in a sample can be used 

 

e.g. buffered charcoal yeast extract agar allows Legionnaires' disease-causing Legionella pneumophila to grow --> and so if this bacteria is present in a sample and combined with buffered charcoal yeast it will grow and multiply, allowing scientists to identify it  

 

Biochemical tests panels:  a series of tests designed to specify a sample’s genus and species 

 

e.g. scientists perform tests such as the Gram stain to determine whether bacteria are Gram-positive or Gram-negative, followed by tests for oxygen requirements (aerobic or anaerobic) and other tests until the species is identified. 

Immunological 

They identify a pathogen by detecting its antigens (proteins on the pathogen) or the antibodies your immune system makes against it --> These methods rely on the specific binding between antibodies and antigens 

ELISA (enzyme-linked immunosorbent assay):  

 

Serology the study of blood serum, typically to determine the presence of antibodies and/or antigens 

 

There are four main types of ELISA tests – direct, indirect, sandwich, and competitive 

 

This is sandwich method 

Step 1: Put antibodies on a plate 

Antibodies specific to a certain pathogen are attached to a plate 
 

Step 2: Add the patient's sample 

The serum sample to be tested is then applied to the plate 

If the pathogen is present, its antigens stick to the antibodies  

 

Step 3: Add a second antibody 

A second detection antibody, linked to a colour-changing enzyme, is added to the plate, binding to any antibody-antigen complexes present 

 

Now the pathogen is trapped between two antibodies. 

This is why it's called a sandwich ELISA. 
 

Step 4: Add the substrate 

A substrate is then added, reacting with the enzyme on the second antibody and changing colour/emitting a signal to reveal whether any pathogenic antigens were present in the sample 

Molecular 

Detects or analyses a pathogen's genetic material (DNA or RNA).  

Hybridisation-based detection 

Labelled segments of genetic material that are complementary to a pathogen’s genetic material are added to a sample 

 

If the pathogen is present: 

The segment sticks to the pathogen DNA. 

Signal = pathogen present 

No signal = pathogen absent 

 

 

Whole-genome sequencing: Provides detailed information about the pathogen 


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  • Direct transmission

  • Indirect transmission


Direct transmission involves contact between an infected person and a susceptible person, either via actual physical contact between them or via close proximity between them 

 

Indirect transmission is disease transmission that occurs without any form of contact or proximity between an infected person and a susceptible person 

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What are the different modes of disease transmission

Transmission route 

Description 

Examples 

 

Airborne transmission  

The spread of pathogens through air via small particles (traditionally <5 µm) that stay in the air for prolonged periods of time after a person sneezes, coughs, exhales, or talks 

  • A person can inhale these particles and become sick even after the original host has left the vicinity. 

Influenza virus – the causative agent of the flu SARS-CoV-2 – the causative agent of COVID-19 Rhinovirus – the causative agent of the common cold 

 

(These are both for airborne transmission and droplet transmission) 

Droplet transmission 

The spread of pathogens through air and contaminated surfaces via respiratory droplets (droplets (traditionally >5 µm) produced by breathing, talking, vomiting, and coughing that could contain pathogens) 

  • They can remain suspended in the air for a short period of time, before falling to the ground/onto a surface --> If a person touches a surface containing droplets and then touches a mucosal surface (such as their eyes, mouth, or nose) the pathogen from the droplet may enter their system and infect them 

 

Direct physical contact transmission 

The spread of pathogens through physical contact between a host and another individual  

  • This contact can occur either via skin to-skin touch, sharing of bodily fluids, sexual contact, oral contact (kissing), from mother to baby in utero or post-birth (vertical transmission), or contact with a contaminated material during some medical procedures (iatrogenic) 

Tinea pedis – the causative organism of athlete’s foot Human immunodeficiency virus (HIV) – the causative agent of acquired immunodeficiency syndrome (AIDS) Epstein-Barr virus (EBV) – the causative agent of infectious mononucleosis (glandular fever)  

Indirect physical contact transmission 

The spread of pathogens via fomites (an inanimate object that, when contaminated with a pathogen, can transmit that pathogen to a new host) (e.g. food, water, tissues, needles) or vectors (an organism that is not affected by a disease but spreads it between hosts) (e.g. Mosquitoes) 

Plasmodium – the causative agent of malaria, spread by mosquitoes  

Faecal-oral transmission 

The spread of pathogens via oral consumption of contaminated faeces 

 

  • Where pathogens excreted in faeces can end up being consumed by another person indirectly via contamination of food or water by infected faeces 

If proper hygiene or sanitation is lacking, the faeces can contaminate: 

  • Food (e.g. if someone doesn't wash their hands after using the toilet before preparing food).  

  • Water (e.g. sewage contaminating drinking water supplies) 

 

  • When a toilet is flushed, especially with the lid open, tiny droplets and particles containing pathogens can become suspended in the air. This is called aerosolisation.  

 

These droplets may:  

  • Land on nearby surfaces such as toilet seats, sinks, taps, or toothbrushes.  

  • Be inhaled or transferred to the mouth via contaminated hands. 

 

 

Vibrio cholerae – the causative organism of cholera Rotavirus – the causative agent of diarrhoea, typically in young children  


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Key strategies in controlling disease transmission 

Prevention 

  • Improving hygiene and sanitation via handwashing  

 

  • Sterilising hands and surfaces/tools using antiseptics (substance that is applied to living tissue to kill or slow the growth of microorganisms) and disinfectants (substance that is applied to non-living materials to kill or slow the growth of microorganisms) 

 

  • Ensuring access to clean water and food  

 

  • Using personal protective equipment (PPE) such as gloves and masks when dealing with sick people  

 

  • Vaccination 

 

  • Lockdown of areas/restrictions to reduce people’s movement and the chance of spreading a disease  

Screening 

  • Routine testing for the presence of disease in a population allows public health workers to quickly see who in a population is affected 

 

  • Officials may observe medication sales at pharmacies and look for changes that might indicate that the prevalence of certain symptoms or illnesses has increased  

Quarantine and isolation 

  • Once a person becomes ill or has the potential to become ill (e.g. is returning home from visiting an affected area overseas), they may be separated from healthy people to ensure they don’t spread their disease 


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  • Antibiotics

  • Antivirals

  • Fungicides


  • Antibiotics are medicines that can be used to treat diseases caused by bacteria by killing or slowing their growth -  they selectively affect bacterial cells by targeting specific biochemical pathways or components unique to bacteria, without damaging the patient’s cells 

 

  • Antivirals are prescription medicines  (pills, liquid, an inhaled powder, or an intravenous solution) that can be used to treat diseases caused by viruses/viral infections --> where they are designed to specifically target viruses, interfering with their ability to attach to, replicate in, and exit from a host cell  

 

  • Fungicides are medicines that can be used to treat diseases caused by fungi/fungal infections --> where they specifically target fungal cells 


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Sometimes antibiotics are used inappropriately, for example by:  

  • Taking antibiotics for viral infections (such as the common cold or flu), even though antibiotics do not work against viruses.  

  • Not finishing the full course of antibiotics.  

  • Taking antibiotics when they are not needed.  

  • Using antibiotics too often


How can this lead to antimicrobial resistance in bacteria

When antibiotics are used incorrectly, not all bacteria are killed.  

  • Most bacteria die.  

  • A few bacteria may have mutations that make them naturally more resistant to the antibiotic 

 

The resistant bacteria survive and reproduce.  

  • They pass their resistance genes to their offspring (and sometimes to other bacteria).  

 

Over time, this can leads to antimicrobial resistance in more bacteria where they are no longer affected by antibiotics 

  • Eventually, the antibiotic no longer works well against that type of bacteria. 


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  • Immunotherapy

  • List and explain the two broad categories of immunotherapy


mmunotherapy is a category of medical treatments that treat disease by modulating/adjusting the immune system 

 

Examples include: 

  • dendritic cell therapy  

  • -CAR-T cell therapy  

  • Antibody therapy  

  • Cytokine therapy 

 

There are two broad categories of immunotherapy:  

  • Activation immunotherapies, which aim to induce or amplify an immune response  

  • Suppression immunotherapies, which aim to prevent or reduce an immune response 


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  • Monoclonal antibodies (mAbs)

  • T or F? Monoclonal antibodies (mAbs) can only treat diseases in a immunotherapeutic way


Monoclonal antibodies (mAbs) laboratory-made antibodies produced by plasma cell clones that bind to a specific antigen 

  • Because of their specificity to one antigen, monoclonal antibodies can be used to target specific types or parts of cells --> e.g. monoclonal antibodies can be used to treat cancer and autoimmune diseases due to their ability to trigger the killing of cancerous or self-recognising cells respectively 


  • False. Monoclonal antibodies can also be used to treat diseases in non-immunotherapeutic ways by treating diseases without modulating the immune system 


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How are monoclonal antibodies produced? (the traditional way - the process that scientists used when they were first producing monoclonal antibodies)

  1. Scientists identify and isolate an antigen that is present on a desired target cell --> this cell will typically be one that is responsible for causing the disease that scientists want to treat 

 

  1. Scientists vaccinate an animal, usually mice, with an antigen --> this vaccination stimulates an immune response against the antigen and results in the selection and proliferation (expansion) of a B lymphocyte that matches the antigen 

 

  1. Scientists extract these B lymphocytes from the spleen of the mice 

 

  1. The extracted B lymphocytes are fused with rapidly-dividing cancerous human plasma cells known as myeloma cells. The products of this fusion are called hybridomas 

    • The reason why these myeloma cells are chosen to fuse with the B lymphocytes is because B lymphocytes do not grow well in vitro (outside living organisms), whereas myeloma cells have the ability to grow indefinitely and produce large quantities of antibodies 

 

  1. Hybridomas are screened so that only the cells with the appropriate antibody are selected --> The hybridomas that produce the specific antibody are cloned, which results in the mass production of these antibodies 

 

  1. Antibodies are then collected and purified before being administered to a patient 


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  • What is cancer

  • How does it occur/spread


Cancer is a complex group of diseases caused by the uncontrolled and unregulated replication of cells that then invade other sites of the body 

  • The most important process in the development of cancer is the accumulation of mutations in a cancer cell’s DNA that allow it to bypass normal regulatory checkpoints of the cell cycle and provide it with survival advantages 

  • Whilst the immune system is normally capable of recognising cells that have developed mutations and destroys them before they have a chance to replicate --> cancerous cells are sometimes able to evade the immune system or develop mutations that allow them to suppress the immune response against them 


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There are two types of monoclonal antibodies used in immunotherapy - identify + describe them

  • naked monoclonal antibodies - monoclonal antibodies that do not have any other molecules attached to them 

  • conjugated monoclonal antibodies - monoclonal antibodies with other molecules (e.g. chemotherapy drugs or radioisotopes) attached to them


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Naked monoclonal antibodies have three main mechanisms of action against cancer cells (just identify it)

  • Antibody-dependent cell-mediated cytotoxicity (ADCC) 

  • Complement activation 

  • Checkpoint inhibition 


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Antibody-dependent cell-mediated cytotoxicity (ADCC)

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Complement activation 

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Checkpoint inhibition  

  • Immune checkpoints are regulators in the immune system that, when activated, suppress the immune system 

  • Whilst suppressing the immune system at times is a normal part of bodily function, some cancer cells secrete molecules that stimulate immune checkpoints, reducing the immune system’s ability to recognise and destroy them 

  • Monoclonal antibodies can be used to block immune checkpoints, meaning the immune system is able to function at a greater capacity and destroy cancer cells more easily 


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What are the other uses of monoclonal antibodies

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Note:

Immunotherapy Vs traditional cancer treatment 

  • Traditional forms of cancer therapy such as chemotherapy and radiotherapy work by directly targeting and killing cells that are rapidly dividing, rather than stimulating the immune system  

  • A large problem, however, is that many other cells of the body – such as hair follicles, and cells lining the mouth and gut – also divide quickly and are killed by these treatments --> this is one of the reasons why people on chemotherapy can suffer from side effects such as hair loss, nausea, and vomiting 

 

  • Whereas antibody-based immunotherapies tend to be more specific and targeted in their attack as monoclonal antibodies have variable regions that bind with cancer antigens specifically, there is a lower chance that other cells in the body will be affected by the treatment and experience side effects 

  • However immunotherapy still can cause a wide array of side effects, and is currently only available as a treatment for very specific types of cancer + it is still typically used in conjunction with traditional cancer treatments such as chemotherapy and radiotherapy


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  • Autoimmune disease

  • How does it occur

  • Examples

  • What do B cells release and T cells become?


Autoimmune disease a disease in which an individual’s immune system initiates an immune response against their own cells 

 

  • Body cells express major histocompatibility complex (MHC) proteins that mark them as ‘self’ 

--> If a person’s immune system is functioning normally, their lymphocytes should recognise these markers and not launch an attack against a cell expressing them 

--> Sometimes, however, lymphocytes fail to recognise these self-markers and end up inducing an immune response against self-cells - resulting in an autoimmune disease 

 

Examples of autoimmune diseases include: rheumatoid arthritis, multiple sclerosis,  type 1 diabetes, and coeliac disease, lupus

 

  • In autoimmune diseases, B cells release autoantibodies (antibodies directed against an organism’s own tissues) and T cells become autoreactive (where they recognise a self-tissue or self-antigen as non-self) 


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Suppression immunotherapies can be used to reduce the immune system's ability to attack self-cells, leading to immunosuppression which is a reduction in the ability of the immune system to generate an immune response 


How can this be done:

This can be done in a few ways, including: 

  • Cytokine inhibition – Cytokines are messenger molecules used by the immune system to coordinate its response --> monoclonal antibodies that bind to and inhibit cytokines can be used to reduce the immune response  


  • B cell and T cell depletion and inhibition – Monoclonal antibodies that bind to autoreactive B and T cells can be used to either inhibit these cells or stimulate other immune cells to destroy them, which reduces the immune system's attack on the body's own tissues


<p><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">This can be done in a few ways, including:</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p><ul><li><p class="Paragraph SCXO74790175 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px; color: windowtext;">Cytokine inhibition – Cytokines are messenger molecules used by the immune system to coordinate its response --&gt; monoclonal antibodies that bind to and inhibit cytokines can be used to reduce the immune response&nbsp;</span><span style="line-height: 20.7px; color: windowtext;">&nbsp;</span></p></li></ul><p class="Paragraph SCXO74790175 BCX0" style="text-align: left;"></p><ul><li><p class="Paragraph SCXO74790175 BCX0" style="text-align: left;"><span style="background-color: inherit; line-height: 20.7px;">B cell and T cell depletion and inhibition – Monoclonal antibodies that bind to autoreactive B and T cells can be used to either inhibit these cells or stimulate other immune cells to destroy them, which reduces the immune system's attack on the body's own tissues</span></p></li></ul><p></p>
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Note:

Immunotherapy Vs traditional autoimmune treatment 

  • The majority of autoimmune diseases have no cure at this point in time --> instead, doctors try to reduce the symptoms experienced by patients 

  • Treatments for autoimmune diseases have normally involved suppressing a patient’s whole immune system via immunosuppressant medications such as non-steroidal anti-inflammatory drugs (NSAIDs) or corticosteroids 

  • This type of broad immunosuppression has meant that these patients become immunodeficient (state which the immune system is no longer able to protect the body against infection or disease) and hence can be more susceptible to developing infections and cancer. 

 

  • Unlike traditional treatments, which suppress the entire immune system, immunosuppression via immunotherapy would be far more specific suppressing only autoreactive cells  (immune cells causing the disease), allowing the rest of the immune system to function normally 

  • Although some immunotherapy treatments are available, they are currently most often used alongside traditional treatments