Hypersensitivity Flashcards
(15 cards)
Allergen features
highly soluble
stable
inhaled or ingested
introduced in low doses
Atopic individual
individual with a genetic tendency to produce IgE to environmental antigens that are otherwise harmless
individuals have lots of IgE, eosinophils and IL-4 secreting TH2 cells
Type I hypersensitivity
AKA allergic reactions
has two stages - sensitisation and response
Sensitisation
allergen penetrates the mucosa
Taken up by dendritic cells that migrate from the tissue to the local LN, and cause naïve t cells to differentiate into th2 cells
TH2 cells produce isotype switching in b cells, which travel back to the tissue
B cells produce antibodies
DOESN’T NECESSARILY PRODUCE SYMTPOMS
Response
cross linking of IgE on mast cells
degranulation of preformed histamine (immediate stage)
late stage: prostaglandins, leukotrienes (inflammatory mediators) and cytokines are produced, eosinophils flood the area
Type II hypersensitivity
antibody mediated binding of Abs to host antigen. two outcomes
- igm or igg binds to own cells, opsonisation
- binding of phagocytes to self interferes with their ability to function (e.g. graves & MG)
Haemolytic disease of the newborn
Rhesus - mother whose first child is rhesus positive = makes rhesus antigens
second child is rhesus positive = antibodies bind to the babies RBCs = lysis
Type III hypersensitivity
complexes of antibody and foreign antigen that aren’t cleared properly
- too much antigen and not enough antibody
Where can immune complexes deposit
joint synovium and vessels: arthritis
blood vessel walls: vasculitis
Type IV hypersensitivity
delayed type
persistent antigens that drive cell mediated response (CD4 mostly)
Stages of Type IV
Sensitisation: dendritic cell primes T cell
response
response: TH1 recognises antigen and releases cytokines, recruiting phagocytes and plasma to site
What causes coeliac disease
tTG2 changes glutamine residues to glutamic acid, makes it more negative (preference at anchor position), making them fit better in the MHC
what MHCs are more likely to get coeliac disease
HLA-DQ2 and HLA-DQ8
Adaptive response to anti gluten antibodies
Anti-gluten antibodies
Anti-gluten CD4+ T cells
anti- TG2 antibodies (produced when B cell takes up entire complex and present gluten on MHC. Get help for T cell specific for gluten while it itself is specific for tTG2)
DTH TH1 cytokines
chemokines recruit macrophages to site, IFNy induces expression of vascular adhesion molecules, activates macrophages, TNF-alpha causes local tissue destruction, IL-3 stimulates monocyte production by bone marrow
