6.3 Immunology

From MaritNy on Quizlet

Primary defence against pathogens

Primary defence against pathogens

Skin and mucous membranes

Thrombin

Clotting factor (Fibrin - fibrinogen)

Thrombosis

Clotting in the coronary artery and remains there (myocardial /infarction)

Phagocytic leukocytes

Eats the pathogen

Phagosome

The vesicle inside of a phagocyte that contains a pathogen.

Hemophillia definition

X-linked recessive disease causing the loss in the ability to form blood clots.

fibrinogen

A soluble protein present in blood plasma, from which fibrin is produced by the action of the enzyme thrombin.

Pathogen definition and example

Disease causing organisms

• Examples:

• Virus

• Bacteria

• Fungi

• Protozoa

Virus

Non-living (need a host cell). Can mutate quickly, has RNA or DNA

eg. HIV, COVID, Flu

Bacteria

Prokaryotes (divide through binary fission)

eg. e.coli and MRSA

Fungi

Eukaryotyes that reproduce with spores

• eg. Athletes foot and ringworm

Antigen

A protein that, when introduced in the blood, triggers the production of an antibody.

Antibody

A globular protein that recognises a specific antigen and binds to it as part of immune response. (triggered by non-self cells) specific to certain antigens. Part of your body.

Immunoglobulins

Antibodies such as IgA, IgE, IgG, IgM, and IgD; secreted by plasma cells (mature B cells) in response to the presence of an antigen.

Transmission methods

Direct contact (Herpes and smallpox - touching the infected area)

• bodily fluids (HIV)

• Animal Vectors (Rabies)

• Blood Contact (Hepatitis)

• Swallowed (Salmonella)

Skin as a protective barrier

• dry thick tough region of dead surface cells

• protects external structures

• biochemical defence - lysosomes (enzymes which break down pathogens)

• pH is slightly acidic not optimal for bacteria (the glands secrete lactic acid)

• Dry, hard to reproduce/ competition

• No openings continuous

Mucous Membranes as a barrier

• normally in the openings (eyes, nose, ears)

• sticky, traps pathogens

• 5.5 pH, not optimal for pathogens

• lysosome

• cillia to aide the removal of pathogens

Blood clotting procedure

• prevents excess blood loss and limit pathogenic access broken blood vessel triggers clotting factors.

• Clotting factors cause platelets to become sticky and adhere to the damaged region.

• Clotting factors also initiate localised vasoconstriction to reduce blood flow.

• Clotting factors also trigger the conversion of prothrombin to thrombin (activating the enzyme)

• thrombin catalysis fibrinogen to fibrin (soluble to insoluble)

• the fibrin forms a mesh of fibers around the cluster of platelets and traps blood cells, forming a clot.

• when the region is repaired - plasmin is activated to dissolve the clot.

Athersclerosis - in terms of 6.3

Atheromes (fat deposits) develop in the arteries are reduce the lumen size.

• this increases pressure, damaging the arterial wall, which is repaired with fibrous tissue, reducing the elasticity of the vessel wall

• lesion called atherosclerotic plaques form in lesions

• if the plaque ruptures --> blood clotting forming thrombus

• if thrombus ruptures it can block smaller arterioles.

Leukocytes - Phagocytes (2nd line of defence)

• chemotaxis attracts the phagocytes to the area of invasion through:

• proteins produces by the pathogen and phospholipids released by the damaged cells.

• the phagocyte attaches to the pathogens' surface protein and engulfs it (endocytosis)

• vessicle is called phagosome

• lysosomes enter the phagosome and break down the pathogen, waste products removed through exocytosis.

• non-specific

Chemotaxis

Cell movement that occurs in response to chemical stimulus

Leukocytes - B-cells and lymphocytes (3rd line of defence)

B-cells: produce antibodies, helper T-cells release chemicals that can activate B cells to produce antibodies.

• antigen presenting cells migrate to the lymph and ctivate specific helper T cells

• The helper T cells release cytokines to activate the particular B cell capable of producing antibodies specific to the antigen.

• the activated b cell divides and differentiates to form short-lived plasma cells that make a high amount of a specific antibody. these antibodies target the antigen

• a small % of the activated B-cell develops into memory cells

Antibody structure

• 4 polypeptide chains to form y-shaped molecules

• the ends are where the antigen binds (called the variable regions)

• the rest of the molecule is consistent w all antibodies

• each type of antibody recongnises a unique antigen

Where do the antigens go in phagocytosis?

The antigens will appear on the surface of the phagocyte. This indirectly activates the T cell which activates the B cell and produces matching antibodies to that antigen. The b cell will differentiate into either a memory cell or a plasma cell. The latter is produced the most and produces the most antibodies. Antibodies bind to the antigens and mark the pathogen. This causes the antibodies to be "markers" on bacteria so phagocytes can find the bacteria and eat it and so that it cannot enter any more cells.

Totipotent

Stem cells with the potential to differentiate into any type of cell. and can therefore cause the expression of different antigens

Clonal selection

The process by which an antigen selectively binds to and activates only those lymphocytes bearing receptors specific for the antigen. The selected lymphocytes proliferate and differentiate into a clone of effector cells and a clone of memory cells specific for the stimulating antigen.

Passive immunity

Antibodies acquired from an outside source, such as another person. No memory cells.

Active immunity

A form of acquired immunity in which the body produces its own antibodies against disease-causing antigens. Memory cells are made.

Antibiotics disrupts:

Cell walls and membranes Protein synthesis DNA synthesis Metabolic processes.

Why antibiotics don't work on viruses

Viruses have a very different structure, therefore they do not work on them, don't have a cell wall, membrane or metabolic processes without a host. Don't work on eukaryotic cells, only prokaryotic, so you do not destroy your own cells.

Antibiotic resistance

Caused by overprescription and overuse, not finishing a full course of antibiotics. Example of evolution by natural selection. Global issue. The mutation naturally arises and divides causing a resistance inside the host, leading antibiotics to be useless. This changes the ALLELE FREQUENCY. Due to natural selection, only resistance survives, causing them to flourish and reproduce. This is hard to eliminate and can spread via plasmids. Hybrid vigour? Most bacteria - good and bad - are affected How to reduce: Use less antibiotics, prescribe with care. Improve sanitation, decreasing spread. Do more research on how to kill bacteria without the risk of a mutation. Take a full course of antibiotics.

Narrow spectrum antibiotics

Treat specific bacteria

Broad spectrum antibiotics

Affect a broad range of gram-positive or gram-negative bacteria

Florey and chain

• looked at penicillin

• Noticed how eye mucus defence did not kill all pathogens.Found penicillin on accident, saw how it killed disease. The essence was extracted, which had no effect on animals but just prokaryotes. -Infected mice with bacteria (strepococus), half were given penicillin and they survived. Then tested on sick humans, most survived.

• this testing is not allowed today

HIV and AIDS

Structure- surrounded by proteins. HAve viral RNA and enzymes inside.

Attacks T-helper cells, binding to the CD4+ protein on their surface, enters via endocytosis, RNA released. Inserts its own RNA into the host cell. Which turns into DNA via reverse transcription. Viral DNA moves to the nucleus, leading to the production of viral RNA, causing viral proteins, complete viruses are released via exocytosis, multiplying. -Mutates in the protein synthesis cause new proteins outside the cells, causing the binding of another receptor, new virus particles are synthesized, during exocytosis these rupture the plasma membrane, killing the cells. When it turns to AIDS

Symptoms: fever, chills, fatigue, nausea, cough w/ phlegm.

Gradually attacks the immune system which is our body's natural defence. This makes it harder to fight off infections and disease. A IDS is caused by HIV, when HIV is advanced. Last stage of HIV when the body can no longer defend itself, very dangerous.

Infected T helper cells are destroyed leading to a reduced number. Since T helpers are needed for B cells and antibodies, antibodies cannot be made. No cure

Virus, inserts its own RNA into the host cell HIV RNA is inserted into the macrophage genome, causing transcription to HIV particles weakens the immune system.

Transmits via: Sexual intercourse Transfusion of blood Pregnancy / childbirth Sharing of dirty needles.