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Flashcards in Immune Responses Deck (9)
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How do Tregs control inflammation?
What is mechanism?

Produce TGF-β and IL-10
Decrease MHC and antigen presentation and inhibit inflammatory cytokines


What is type 1 hypersensitivity?

IgE acts in mast cells to cause release of granules
Driven by Th2 cytokines
Second exposure is the allergic reaction. In first one the antibody is made.


What are clinical effects of allergic reaction?

Vascular permeability increased
Smooth muscle contraction
Mucus production


What happens in anaphylaxis?

Extreme allergic response
Massive histamine and TNFα release results in drop in blood pressure, swelling of throat and mucus membranes and respiratory collapse


What is type 2 hypersensitivity?

Antibody dependent cytotoxicity
E.g. Complement dependent red blood cell degradation


What is type 3 hypersensitivity?

Autoantibodies destroy host cells
5 mechanisms:
1) antibody medication activation of complement
2) auto antibody mediated opsonisation
3) autoantibodies and complement mediated neutrophil recruitment
4) auto antibody dependent cell-mediated cytotoxicity
5) antireceptor autoantibodies


What are the three pathways form complement activation?

Classical; antigen:antibody complexes
MB-lectin pathway; lectin binds to pathogen surface
Alternative pathway ; antibodies against pathogen surfaces


What happens to small immune complexes?

Excess small antigen immune complexes cannot fix complement so are instead taken up into tissues .
This can effect the tissue;
In skin: arthus reaction
In synovial fluid: arthritis
In kidney glomerulus : glomerulonephritis
In epithelium of blood vessels: vasculitis
In joints: SLE


What is type 4 hypersensitivity?
What are the three syndromes?

Only one mediated by T cells
1-3 days to occur due to T cell maturation time and need large dose of antigen