When Thing Go Wrong with the Immune System pt. 2 Flashcards
Gell and Coombs classification of hypersensitivies
Type I, II, III and IV. Types can overlap.
Hypersens. types with relevance to allergic diseases
Type I and II
Sensitization
First exposure that induces an often weak or transient immune response
Type I
IgE mediated.
IgE mediated hypersens.
Cross-linking of FcE receptor on mast cells by antigen-binding on IgE causes degranulation
Type II
New epitopes on cell surfaces makes them target of antibody mediated immune attack
Type III
Soluble self antigen causes formation of immune complexes
Serum sickness
Systemic type III HS following intravenous adiminstration of antigen.
Type IV
T cell (TH2, TH1, CTL) mediated self reactivity, causing inflammation or cell death.
Immune development
Maturation of immune components, beginning short after conception and continuing after birth.
Th1 status in utero
Repressed due to mother’s Th2 bias. Failure to correct after birth can give elevated risk of allergy and other diseases.
Atopy
Tendency to manifect local hypersensitivities. Defined as tendency to produce IgE.
Mast cell response
Release of enzymes and toxic mediaters such as tryptase, histamine and heparin.
Recruitment of cells by Il-4 or Il-5, TNFα etc.
Allergic rhinitis and hay fever are examples of…
Local type I HS.
Immediate type HS1
If sensitization already found place, the response to the antigen is immediate and followed by a late phase response.