Chapter 21 Flashcards New

1.     What protein I the skin gives it a waterproofing waxy element?

keratin

Two halves of the immune system

a.     __________, which is nonspecific

b.    _________, which is specific (adapts to things you’ve been exposed to)

Innate immunity

Adaptive immunity,

Innate defenses

1. The innate side of our defense is concerned with preventing the _____________ in our body

2. It is further divided into two portions

a. The first line of defense - ____________

1. Includes ______________

b. The second line of defense - __________________________

Innate defenses

1. The innate side of our defense is concerned with preventing the entry and spread of pathogens in our body

2. It is further divided into two portions

a. The first line of defense

i. Barriers that prevent the entry of pathogens

1. Includes skin, mucous membranes (lining anus, vagina, nose, etc)

b. The second line of defense

i. Proteins, phagocytes and other cells that prevent the spread of any pathogens that make it past the first line barriers

What is the first line of defense?

Physical and Chemical Barriers

Surface Barriers

Physical Barriers: _____1_____

Chemical barriers: ___4 ____

The skin

i. Acid (the acid mantle) – lining that has a very low pH —Will physically break things down

ii. Enzymes (primarily lysozyme)

1. Lysozyme – enzyme found in saliva, tears, etc, that helps break bacteria and fungi in those areas down

iii. Mucin — Protein that turns into mucous when it comes into contact with water; Becomes thick and slimy that things get trapped in

iv. Defensins (antimicrobial peptides and proteins) - Small proteins that have defensive properties, located on the surface of skin, inside mouth and nose, etc.

What are the innate internal defenses? (Second Line)

Includes 6

Pattern Recognition Receptors

Phagocytes (Neutrophils, Macrophages)

NK cells

Inflammation

antimicrobial proteins

fever

a.     What are pattern recognition receptors?

i. Substances on the surfaces of bacteria (different for each pathogen, but have a similar pattern), that allows our body to recognize it as a pathogen that shouldn’t be there based off of how it is shaped

Phagocytes

Phagocytosis of bacteria

ii. Macrophages (_________ once they leave the blood stream)

2. Phagocytosis – ___________

3. Opsonization – _________________

monocytes

eats things that do not belong

something on a cell or other substance that enhances phagocytosis (makes it easier and more likely)

a. Natural killer cells (NK cells)

i. A special type of ___________

ii. Induce _________in target cells

1. NK cell releases substance on cell and it responds by making a lot of __________ until it _____________

iii. Enhance __________

a. Natural killer cells (NK cells)

i. A special type of lymphocyte____

ii. Induce apoptosis (cellular suicide) _in target cells

1. NK cell releases substance on cell and it responds by making a lot of lysozomes until it ruptures/eats itself

iii. Enhance inflammation - inflammation is our immune system at work

What are the 4 cardinal signs of inflammation

1. _____Redness___

2. __Heat_

3. __Swelling_

4. Pain

Inflammatory Chemical Release:

Mast cells - release ___________, which causes inflammation

Other chemicals like _______ can also cause inflammation

histamine

heparin

Mast cells that cause inflammation → _____ and increased ________of capillaries (allows more ___________)

1. __________ – excess blood coming to the area (causes redness and heat)

2. ______ – the increased permeability of capillaries means more fluid can leak out. The fluid is called ________. Similar to plasma but has clotting factors and antibodies

3. ________ – tissue swelling that causes pressing on nerve endings (which causes pain), but this pressing pushes lymph away into the lymphatic system, which we want

Mast cells that cause inflammation →vasodilation and increased permeability of capillaries (allows more blood to that small area)

1. Hyperemia – excess blood coming to the area (causes redness and heat)

2. Exudate – the increased permeability of capillaries means more fluid can leak out. The fluid is called exudate. Similar to plasma but has clotting factors and antibodies

3. Edema – tissue swelling that causes pressing on nerve endings (which causes pain), but this pressing pushes lymph away into the lymphatic system, which we want

i. Phagocyte mobilization

1. Leukocytosis –

2. Margination –

3. Diapedesis –

4. Chemotaxis –

i. Phagocyte mobilization

1. Leukocytosis – leukocytes start to multiply and enter blood from bone marrow

2. Margination – the leukocytes start to crawl along the walls of the blood vessel as they get close to the site of breach

3. Diapedesis – leukocytes squeeze out of the gaps along the wall in between the cells, the most permeable part of the blood vessel

4. Chemotaxis – response to a chemical (in this case its positive chemotaxis, where cells are attracted toward a chemical). The WBCs are attracted and once they get to the area, they start cleaning the area of debris and bacteria they run into

Interferons =

response to virus infections

How viruses work:

Only the ________ enters the cell, the rest of the virus is __________

genetic material

disposable

How does interferon work

• infected cell realizes something is wrong

• it produces interferon (signaling protein) and secretes it into the surround interstitium

• travels to the neighboring cells and they produce AVP, which blocks ribosome

• viral dna/rna gets degraded

i. Complement (Antimicrobial) proteins – a bunch of individual proteins that when activated by something _____________, start to ______________ Depending on which ones stick to which other ones, there are different results

invading our body,

stick together

Complement Proteins

a. Opsonization – makes __________ easier and more likely

i. ______how does that happen?________

b. Enhanced ________________

c. Membrane attack complexes (MACs)– occurs on the cell membrane of some sort of pathogen; the compliment proteins ___________ and form a _____ within the ________ that allows __________ into the pathogen and the bacteria _____________

a. Opsonization – makes phagocytosis easier and more likely

i. Stick to a pathogen so that a macrophage can grab onto them (the compliment proteins) and its easier for phagocytes to pull it in

b. Enhanced inflammation – makes inflammation stronger

c. Membrane attack complexes (MACs) or “holes in the pathogen” – occurs on the cell membrane of some sort of pathogen; the compliment proteins come together and form a ring within the membrane that allows water from the tissues into the pathogen and the bacteria swells until it lyses

Fever:

i. In response to foreign agents, ________ is released by leukocytes and macrophages

1. These chemicals increase our body’s thermostat (by telling the ___________ to increase our body temp) ____

2. Liver and spleen pull _____________ from the blood stream and hold onto them for a while (this is helpful because bacteria need them)

i. In response to foreign agents, ___pyrogen is__ released by leukocytes and macrophages

1. These chemicals increase our body’s thermostat (by telling the hypothalamus to increase our body temp) ____

2. Liver and spleen pull iron and zinc from the blood stream and hold onto them for a while (this is helpful because bacteria need them)____

How do innate immune cells know if a cell is foreign?

- They use pattern recognition receptors - Substances on the surfaces of bacteria (different for each pathogen, but have a similar pattern), that allows our body to recognize it as a pathogen that shouldn’t be there based off of how it is shaped

For adaptive immunity, we much first _____________

be exposed to the pathogen

Adaptive immunity is divided into: (explain both)

Cell Mediated Immunity and Humoral immunity

a. Cell-mediated immunity

i. Concerned with cells that have already been affected (virus gets in, ell becomes cancerous, etc) _

b. Humoral immunity (antibody-mediated immunity)

i. Concerned with pathogens in our “humors” (body fluids), Meaning they have not yet gotten inside of our cells _

1. Classification of immunities by stimulus

a. Natural active -

b. Artificial active -

c. Natural passive -

d. Artificial passive -

1. Classification of immunities by stimulus

a. Natural active - occurs when you are exposed to a live pathogen, develop the disease, and recover. Your immune system responds by producing antibodies and memory cells.

b. Artificial active - Achieved through vaccination. Vaccines contain dead or weakened pathogens or their components, prompting your immune system to produce antibodies without causing the disease.

c. Natural passive - Occurs naturally when antibodies are transferred from mother to child, either through the placenta during pregnancy or through breast milk after birth.

d. Artificial passive - Involves the injection of antibodies from another source, such as gamma globulin injections, to provide immediate protection

Antigens are _____________

substances that can provoke an immune response

Cells of the adaptive immune response

1. T-lymphocytes (T-cells) - oversee ___________

2. B-lymphocytes (B-cells) - antibody-producing lymphocytes that constitute the cellular arm of adaptive immunity.

3. Antigen-presenting cells (APCs)

a. Not specific like B and T cells

b. Only play an auxiliary role in cell-mediated immunity

c. Major Histocompatibility Complexes (MHCs)

Cells of the adaptive immune response

1. T-lymphocytes (T-cells) - oversee humoral immunity.

2. B-lymphocytes (B-cells) - antibody-producing lymphocytes that constitute the cellular arm of adaptive immunity.

3. Antigen-presenting cells (APCs)

a. Not specific like B and T cells

b. Only play an auxiliary role in cell-mediated immunity

c. Major Histocompatibility Complexes (MHCs)

Cells of the adaptive immune response

1. T-lymphocytes (T-cells) - oversee __________

2. B-lymphocytes (B-cells) - produce _____, present T-cells with_________, form _____________cells

3. Antigen-presenting cells (APCs)

a. Not ________ like B and T cells

b. Only play an auxiliary role in cell-mediated immunity

c. Major Histocompatibility Complexes (MHCs) - type of ___________

Cells of the adaptive immune response

1. T-lymphocytes (T-cells) - oversee humoral immunity.

2. B-lymphocytes (B-cells) - produce antibodies, present T-cells with foreign pathogens, form effector and memory cells

3. Antigen-presenting cells (APCs)

a. Not specific like B and T cells

b. Only play an auxiliary role in cell-mediated immunity

c. Major Histocompatibility Complexes (MHCs) - type of self-antigen

Maturation of T and B cells

a. Location of Maturation for T or B Lymphocytes –

b. Immunocompetence (T-cells) – we want to make sure these cells _____ and ______ to _________

c. Positive selection (T-cells) – make sure the cells recognize the___________________(if they don’t, they do not continue to mature)

d. Self-tolerance (T-cells) – we don’t want them to recognize any self antigens except for ________________, recognizing ____ from ________

e. Negative selection (T-cells) – make sure they do not recognize any other self-antigens, Eliminate self-reactive T cells that could cause __________

a. Location of Maturation for T or B Lymphocytes – B lymphocytes (RBM), T lymphocytes (Thymus)

b. Immunocompetence (T-cells) – we want to make sure these cells recognize and respond to foreign antigens

c. Positive selection (T-cells) – make sure the cells recognize the special major histocompatibility complex (if they don’t, they do not continue to mature)

d. Self-tolerance (T-cells) – we don’t want them to recognize any self antigens except for major histocompatibility complex, recognizing self from non-self

e. Negative selection (T-cells) – make sure they do not recognize any other self-antigens, Eliminate T cells that could cause autoimmune diseases.

once cells are fully matured but have not yet encountered their ___________ (most hang out in the ___________, but can be anywhere in the body)

once cells are fully matured but have not yet encountered their specific foreign antigen (most hang out in the lymph nodes, but can be anywhere in the body)

Foreign antigen encounter typically occurs in the __________

b. Clonal selection –

lymph nodes

b. Clonal selection – special type of mitosis that occurs when a naïve cell encounters its specific foreign antigen – makes lots and lots of copies (causes lymph node swelling when sick)

Clones come in 2 types:

i. Effector cells – the ones that fight the current infection

ii. Memory cells – not active during the initial infection (they go and hide)

Types of APCs: (4)

1. Dendritic cells – in the skin (neighborhood watch) – these are the most effective/often used APCs.

a. Dendritic cells are part of innate immunity, so they are non-specific.

b. They either phagocytize the pathogen or release chemicals on the pathogen, while also tearing off a piece of the foreign antigen to go show to a naïve T-cell. The T-cell then goes and finds it.

2. Macrophages – monocytes that have left the bloodstream and moving through the tissues

a. If they encounter a foreign antigen, they do the same thing

3. B-cells – find a pathogen and find a (special type of T-cell) helper T-cell.

4. reticular cells – form stroma that makes up lymphoid organs

What do all APCs do?

all have encountered something that does not belong in the body, tore a piece of it off, and they go show the cells of the adaptive immune system(AIS) the shape of the foreign antigen, telling the AIS what to look for

Activation of humoral immunity must result from a

free antigen (in the body but not yet inside the cells)

1. Differentiation

a. Can be sped up by ___________

b. Effector cells called ___________

i. Mode of action secrete ___________ in the _________________

c. Memory B cells:

i. During the primary immune response – happens after a delay of almost a_______; antibodies are made by the ____________ but youre still very sick

ii. Secondary immune response – as soon as a memory b-cell encounters its specific foreign antigen, it immediately becomes a __________and becomes a lot of __________.

1. These cells stay in circulation a lot longer (often for life)

1. Differentiation

a. Can be sped up by helper T cells as we will see later

b. Effector cells called plasma cells _

i. Mode of action secrete antibodies in the current/ongoing infection_

c. Memory cells

i. Primary immune response – happens after a delay of almost a full week; antibodies are made by the newly cloned B-cells/ plasma cells but youre still very sick

ii. Secondary immune response – as soon as a memory b-cell encounters its specific foreign antigen, it immediately becomes a plasma cell and becomes a lot of antibodies.

1. These cells stay in circulation a lot longer (often for life)

What is the difference between active and passive humoral immunity?

a. Active – antibodies were made by your own body

b. Passive (someone or something else made the antibodies)

Antibodies: don’t kill anything themselves but ____________

tag things to be killed

Antibodies:

i. Neutralization –

ii. Agglutination* -

iii. Precipitation –

iv. Compliment activation –

v. Opsonization** -

i. Neutralization – bind to antigens on surface of the cell and by covering them, the bacteria cannot harm you

ii. Agglutination* - cause RBCs/bacteria to stick together

iii. Precipitation – antigens bind with antibodies to form ladder structures that precipitate out of the blood

iv. Compliment activation – causes lysis

v. Opsonization** - enhances phagocytosis

Cell mediated immunity is concerned with cells that ________

have something wrong with them

a. Virus/bacteria

b. Cancerous

c. Transplanted

T Cell Names

a. Helper T-cells (TH) (CD4)

i. ___ is naïve – called a ___ cell prior to encountering its specific antigen (name comes from the receptors on the surface)

ii. ____________ is activated – once the cell encounters it specific foreign antigen

b. Cytotoxic T-cells (TC) (CD8)

i. _____ is naïve – name comes from its receptor,

ii. _____________ is the activated form

c. Regulatory T-cells (Treg) (Suppressor T-cells) (Tsup) – these are ALL the same thing, just many different names

i. A special type of CD4/Helper T-cell

a. Helper T-cells (TH) (CD4)

i. CD4 is naïve – called a CD4 cell prior to encountering its specific antigen (name comes from the receptors on the surface)

ii. Helper T cell (TH) is activated – once the cell encounters it specific foreign antigen

b. Cytotoxic T-cells (TC) (CD8)

i. CD8 is naïve – name comes from its receptor,

ii. Cytotoxic (T-cell) is the activated form

c. Regulatory T-cells (Treg) (Suppressor T-cells) (Tsup) – these are ALL the same thing, just many different names

i. A special type of CD4/Helper T-cell

1. MHCs - Major Histocompatibility Complexes – type of _________

a. Class I – found on ______

b. Class II – found on _________

1. MHCs - Major Histocompatibility Complexes – type of self-antigen

a. Class I – found on every nucleated cell in the body

b. Class II – found on antigen presenting cells only

Activation of Helper T-cells

• Naive CD4+ T-cells circulate and scan for antigen: Many CD4 helper T-cells approach the foreign antigen (bacteria, virus, etc.). They keep testing until one specific T-cell’s receptor “fits” the antigen perfectly. However, because the T-cell is still naive, nothing happens yet—no activation.

Macrophage/APC engulfs the pathogen:

• The macrophage (an antigen-presenting cell, or APC) comes along and eats/phagocytoses the foreign antigen.

Antigen processing and presentation on MHC II:

• Inside the macrophage, the antigen is broken down. A piece of it is moved onto MHC II, which is on the cell surface.

• The MHC II now displays the antigen fragment, ready to be shown to T-cells.

CD4 T-cell receptor (TCR) binds the complex:

• A CD4 T-cell with the matching receptor comes along

• Once it does, an arm of the CD4 will reach around, feeling for the MHC II. Once the arm feels the MHC II, the other piece of the receptor (shaped for a specific antigen), fits with the antigen and matches the shape.

• This confirms the match: TCR fits the antigen and CD4 locks onto MHC II. This binding of both the MHC II and the receptor to the antigen, starts the activation process.

Macrophage/APC releases Interleukin-1 (IL-1):

• The APC senses it is being “inspected” and releases Interleukin-1 onto the docked CD4 T-cell. This finalizes the activation of the naive helper T-cell.

Clonal selection / expansion occurs:

• Memory helper T-cells are produced → they hide in the body for long-term immunity (faster response next time).

• Active/effector helper T-cells (Th cells) are produced in large numbers.

• Active helper T-cells T_H (the effector cells) release Interleukin-2

• IL-2 acts like an alarm call / signal (“tattle-tale”) to the rest of the immune system: “Foreign antigen detected — everyone fight!”

• It activates B-cells, cytotoxic T-cells, macrophages, etc.

• Naive CD8+ T-cells circulate and scan for antigen:
  Many CD8 cytotoxic T-cells approach body cells displaying MHC I. They keep testing until one specific T-cell’s receptor “fits” the presented antigen perfectly. Because the T-cell is still naive, nothing happens yet.

• Target cell displays MHC I (normal or abnormal):
  Every body cell constantly puts MHC I on its surface (proteins are quickly degraded and replaced).

  • In a cancerous cell: energy goes to rapid division, so MHC I is made irregularly or misshapen.

  • In a virus-infected cell: the cell is busy making viruses, so pieces of viral protein get stuck to the new MHC I and are displayed on the surface. MHC I therefore shows two things: “I am self” + “something is wrong inside” (misshapen = possible cancer; viral piece = infection).

• CD8 T-cell receptor binds the MHC I complex:
  A CD8 T-cell with the matching receptor comes along and docks onto the MHC I + abnormal antigen on the target cell.

• CD8 co-receptor “feels” for MHC I (second confirmation):
  The arm of the CD8 molecule reaches around and binds directly to the MHC I.
  This double binding (receptor + CD8 arm) confirms that the cell is presenting something abnormal.

• CD8 begins activation but needs help from helper T-cells:
  Once recognition occurs, the CD8 T-cell is partially activated but cannot yet divide.
  It must first find an activated helper T-cell (from the CD4 pathway).
  The CD8 shows the helper T-cell the pathogenic antigen it has detected.
  The helper T-cell then releases Interleukin-2 onto the CD8 cell.
  Interleukin-2 is the final signal that allows the CD8 to fully activate and proliferate.

• Clonal selection / expansion occurs:
  The activated CD8 T-cell divides into:

  • Memory cytotoxic T-cells (Tc) → they leave and hide for long-term immunity (faster response next time).

  • Effector cytotoxic T-cells (Tc) → these are the active killer cells produced in large numbers during the current infection.

• Effector cytotoxic T-cells kill the target cell:
  The active Tc cells release:

  • Perforin → pokes holes in the target cell’s plasma membrane.

  • Granzyme and lymphotoxin → enter through the holes and trigger apoptosis (programmed cell death).

  • Interferon and Tumor Necrosis Factor (TNF) → additional signals that are anti-viral and anti-cancer.

  The cytotoxic T-cell itself does not get infected or harmed; it simply destroys the abnormal cell.

Role of Regulatory T-cells (explain

i. Helper T cells activate the immune system by signaling “something’s here—we need to get into fight mode.” This puts the body into an active state where the immune system releases chemicals to attack anything that doesn’t belong.

ii. If this fight mode continued indefinitely, it would eventually start harming the body’s own tissues. To prevent that, helper T cells are on a built-in timer. As time passes, they change and become regulatory (suppressor) T cells.

iii. These regulatory T cells then release chemicals that say “stop fighting.” Their job is to turn the immune system back off and take it out of fight mode. This is necessary so the body does not eventually destroy its own tissues.

What do defects of regulatory t-cells cause?

a. Defects - types of autoimmune diseases result from regulatory T cells that are not active enough. When regulatory T cells are not active enough, the immune system stays in fight mode (instead of being turned off by the suppressor chemicals they normally release). As a result, the body actually starts damaging some of its own tissues.

Transplants and immunosuppression

1. Drugs suppress cells that divide rapidly such as _________________

a. This means that there are ______________

Transplants and immunosuppression

1. Drugs suppress cells that divide rapidly such as leukocytes (like lymphocytes)_

a. This means that there are no defenses against sickness

HIV/AIDS

explain reverse transcriptase

ii. Why haven’t we been able to vaccinate or target the virus?

b. Target cells of HIV

ii. Reverse transcriptase – because all living things normally transcribe RNA from DNA (DNA→RNA), but retroviruses do the opposite (reverse transcription)

1. Because the cell isn’t equipped to make DNA from RNA, the transcription gets messed up, resulting in viruses (and in turn, antigens) that look a little bit different every time. As a result, the body is constantly looking for the former version of the antigens, not the new, changed version

attaches to CD-4 receptors on helper T-cells, stop doing what theyre supposed to and keep making copies of the virus

i. No helper T cells → immune system isn’t turned on

i. HIV doesn’t kill, but because it _____________, it turns things (like a cold) that is harmless to most, into ________

i. HIV doesn’t kill, but because it turns off the immune system, it turns things (like a cold) that is harmless to most, into something fatal

• Allergens are a type of _______.

• Allergies happen because of a “miscommunication” — your immune system mistakenly thinks the harmless allergen is dangerous.

• antigens on mast cells and basophills → triggers release of large amounts of ________

antigen

histamine