Type III & IV hypersensitivity & autoimmunity Flashcards Preview

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Flashcards in Type III & IV hypersensitivity & autoimmunity Deck (15):

Type III H aka

Immune complex hypersensitivity or clumping
I=acId or C=abCd


how does Type III H work?

Ab+Ag forms AgAb (immune complex) and it is deposited
-usually deposited on endothelium d/t slow flow such as in kidneys (glomerulonephritis)
-when it attaches the complement and basophils and neutrophils will remove it which leads to damage
-inflammation and tissue damage follows


examples of Type III H

glomeulonephritis and rheumatoid arthritis
-in rheumatoid arthritis the immune complex deposits in joints and inflammation is caused when the IC is removed by complement as it damages not only the IC but also whatever cell it is attached to


Type III Immune COmplex H (._______?) why is this word used?

-clumps form when we make enough Ab to bind to the Ag but not enough Ab to get rid of the Ag
-these clumps cause problems when they settle in joints or the small blood vessels in the kidney


2 reasons why immune complex isnt removed during Type III H

1-some are insoluble
2-not recognized by enzymes (too small)


Type IV aka

T cell mediated H OR delayed H


Type IV H is mediated by

cell mediated not Ab mediated


Type IV. how does it work

T cell mediated H or delayed H (TYPE IV)
-macrophage presents Ag to T cell--T cell is sensitized--cytotoxic T cells--T cells destroy Ag bearing cells--inflammation and damage


2 types of T cell mediated H or delayed H

-1-direct (stat)
((even if a virus has no cytotoxic effects eg hepatitis it will still kill))
-2-Delayed (days) needs time to produce lymphokines eg TB test where we waited 2 days until the reaction
eg contact dermatitis with poison ivy which takes 2 days to appear?


How are T cell mediated H and Delayed H different

fig 19-6
Primed CD4 cells (TH) activate CD8 (TC) cells which target cells by direct toxicity and activate CD4 (TH) which releases cytokines.
Cytokines are what produce the delayed H response whereas the TC cell produces the direct cell mediated cytotoxicity


how does autoimmunity occur?
what results from this?

self Ags are normally tolerated but when this tolerance is lost the self is considered foreign
-Abs will target self Ags
-Ab+Ag--inflm, damage and necrosis


how can self tolerance be lost? and you end up with autoimmunity

1=abnormal T cell acitivity
2=molecular mimicry
3=expoure of previously masked self Ag


autoimmunity: if you have abnormal T cell activity what could occur

eg no T cell suppression they can run wild and cause damage
(most likely when not enough its immunodeficiency?)


autoimmunity: what does molecular mimicry entail?

when there is similarity in the epitope there is a mistaken identity
-similarity in one area of the protein molecule (the epitope) results in confusion and destruction despite it being self


autoimmunity: how is a previously masked self-ag exposed that previously wasnt. describe this process

eg by disease such as SLE (systemic lupus erythematosis. Ags targeted are the nuclei and therefore almost all cells of the body

-during embryogenesis the exposed Ags are gradually incorporated into the tissues and structures and no longer exposed. Because the immune system isnt dev. yet it wont recog the self Ags when theyre exposed by disease and therefore it will destroy them