Flashcards in Allergic Disease Deck (44)
Undesirable, damaging or discomfort producing reactions produced by the normal immune system, directed against inocuous antigens in a pre-sensitised (immune) host
Type II hypersensitivity
Immunopathogenesis of Type II hypersensitivity
IgG/IgM Ab response against combined self/foreign antigen at the cell surface-complement activation/phagocytosis.
Clinical features for type II hypersensitivity
Mins to hours. Cell lysis and necrosis.
Common antigen for type II hypersensitivity
Associated diseases with type II hypersensitivity
erythroblastosis fetalis, goodpasture's nephritis. Rh reaction with mother/foetus.
Type III hypersensitivity reaction
Immunopathology of type III hypersensitivity reaction
IgG/IgM Ab against soluble antigen-immune complex deposition.
Clinical features of type III hypersensitivity
Onset 3-8 hours. Vasculitis.
Traditional cause for type III hypersensitivity reaction
Associated diseases for type III hypersensitivity reaction
Type III reaction to IV route of antigen
Vasculitis, arthritis, nepthritis
Type III reaction to SC route of antigen
Arthus reaction-perivascular area
Type III reaction to inhaled route of antigen
Type IV hypersensitivity reaction
Delayed- no Ab involved
Immunopathology of type IV hypersensitivity
Antigen specific T cell mediated cytotoxicity
Clinical features of type IV hypersensitivity
Metals e.g. nickel (tuberculin reaction)
Associated diseases of type IV hypersensitivity
Immunopathology of type 1-anaphylaxis IgE mediated hypersensitivity
Increased IgG levels
Tissue inflammation with eosinophils, mastocytosis, basophil infiltration.
Presence of CD4 cells secreting Il4, Il5, Il13
More exposure to infections, less allergies. Mechanisms is Th1-Th2 deviation (Th1-infection, Th2-allergy)
Association between genetics and rhinitis
None, as opposed to asthma and atopic dermatitis
What happens to the T cell activation in allergic reactions
Treg pathway suppressed, Th1 and Th2 pathways are activated.
IgE Abs are induced by which cytokines?
B cells activated by Th2 cells-produce IgE Abs, induced by Il-4 cytokines
What happens when an allergen is in contact with a pre sensitised host?
Antigen binds to fab region of IgE on sensitised mast cell, triggering the release of vasoactive amines.
Immunopathogenesis of type I hypersensitivity
IgE Ab mediated mast cell and basophil degranulation-release of preformed and de novo synthesised inflammatory mediators.
Clinical features of tyep I hypersensitivity
fast onset (15-30 mins) wheal and flare
Late phase response of type I hypersensitivity
Eosinophils, central role for Th2 T cell
Describe the initial response of the mast cell in type I hypersensitivity, following antigen binding to IgE on surface of mast cell
Degranulation-histamine, proteases, chemotactic factors