Hypersensitivity/allergy L4 Flashcards
(40 cards)
What are the 3 cayses of hypersensitivity
Allergy, reactions to infections, autoimmune diseases
What are type 1,2,3 from
Antibody mediated, sometimes via th2 response
What is thpe 4 mediated by
Delayed t cell responses , 17,1,cd8
What hppens on first exposure in type 1
Pamp from allergens like pollen in hay fever can cause actication of apc like dc and macrophages. Apc allows th2 differentiation. Th2 then via TD responses binds b cells via cd40, secretion of il4,il13 can cause class switching to ige, mast,baso and eosinophil attraction too
Ige then binds fcr e on the mast or basophils causing it to be sensitised for secondary exposure
Which cytokines from th2 ade important in th2 ewsponse and ige response in type 1 hypersensitivity
Il4,13 and 5 for eosinophil production
What are mast or basophils exposed to ige on fiest exposure
Sensitised for secondary eg pollen again
What happens on secondary exposure
Instanr degranulation of things like tnf a, histamine
Lipid production of things like pgd2
All cause inflammation eg in airway
Where are type 1 allergens usually found and give examples
Mucosal surfaces
Wg food, pollen, drugs
What types of genetic polymorphisms can affect hypersensitivity type 1
Mhc, il 4, fcr e on mast and basophils
Which ab are made against alletgens in type 2 which mediate hypersensitivity
Igg and igm
Where are allergens in type 2 found
Cell bound eg rh on rbc
How does complement have a part in type 2
Gets actucated by igg and igm via c1q, produces opsin coating the cell with allergen on it for phagocytosis.
Also mac which kills the cells too
What other yype of ab mediated killing in type 2 to innocent cells
Adcc via fcr on cells like eosinophils and nk cells which then kill the cells cia granules
What are frustrated phagocytes and how does this cause tissue damage in type 2
When they try engulf the complement or ab coated cells with allergens on them via fcr or c3b recetors. Too larhe fells cause release of lysosomal products = tissue dmaage
Explain haemolytic disease of newborn as a type 2 example
If a chuld has rh ag on their rbc and mother is nevstice. She makes anti rh in her first pregnancy. Usually igg. On second pregnancy, anti rh will cross placenta and fix complement and themselebs on rbc causing the killing of rbc = anemia
What causes brain damage in haemolytic disease
Hg breakdown into billirubin
What treatment is used for haemolytic disease
Uv to interfere with billirubin
Ab which bund rbc wne block anti rh
How can drugs inruce haemolytic diaease
Can bind rh which then attract ab for the frugs
Ehat is responsible for type III eg RA
Igg complex with soluble allergens to form immune complexes (ICs)
What happens to ICs not cleared
Deposited on tissue causig damage, inflammation and blockage wg of kidney
Which size ICs are good and why
Large ic can be removed by complement activation wnd therefore c3b qnd mac mediated removal
What do small ic bind to which causes mast cell degranulation causing problems
Fcr y on mast or basophils
What happens when small ics bind to neutrophils via fcr y
Cant be phagocytosed well. Causes rekease of lysosomal content for tissue damage
What happens if the small ic bind macrophages
Macrophage pahgocytosis releases inflammatory cytokines and other mediators of inflammation