Immune response that results in bystander damage to the self
Type I - Immediate hypersensitivity
Onset - seconds
IgE-mediated antibody response to external antigen
Sensation stage: production of specific IgE by B cells (helped by T cells) in response to initial allergen exposure, residual IgE antibodies bind to circulating mast cells via Fc receptors
Allergic stage: on re-exposure to allergen, the allergen will bind to IgE coated mast cells → cell degranulation (release of histamine and other inflammatory mediators)
Clinical examples - asthma, hay fever, food allergy (→ anaphylaxis)
Type II
Onset - seconds/hours
IgM or IgG antibodies bind to antigens on the cells of particular tissue types → complement system activation, or antibody dependent cell-mediated cytotoxicity (e.g. by NK cells)
Clinical examples:
Goodpasture’s syndrome: autoreactive antibodies to type IV collagen bind to the basement membranes of alveoli and glomeruli → alveolar haemorrhage, kidney disease
Grave’s disease: autoreactive antibodies bind to the TSHR → hyperthyroidism
Type III
Onset - hours
Antibody binds to excess soluble antigen (in circulation) producing small immune complexes which are trapped in small blood vessels, joints and glomeruli → activate complement → attracts inflammatory cells
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