Type | Description | Mechanism | Clinical features |
I Immediate reaction (within one hour) | IgE-mediated, immediate-type hypersensitivity | Antigen exposure causes IgE-mediated activation of mast cells and basophils, with release of vasoactive substances, such as histamine, prostaglandins, and leukotrienes. | Anaphylaxis Angioedema Bronchospasm Urticaria (hives) Hypotension |
II | Antibody-dependent cytotoxicity | An antigen or hapten that is intimately associated with a cell binds to antibody, leading to cell or tissue injury. | Hemolytic anemia Thrombocytopenia Neutropenia |
III | Immune complex disease | Damage is caused by formation or deposition of antigen-antibody complexes in vessels or tissue. Deposition of immune complexes causes complement activation and/or recruitment of neutrophils by interaction of immune complexes with Fc IgG receptors. | Serum sickness Arthus reaction |
IV | Cell-mediated or delayed hypersensitivity | Antigen exposure activates T cells, which then mediate tissue injury. Depending upon the type of T cell activation and the other effector cells recruited, different subtypes can be differentiated (ie, types IVa to IVd). | Contact dermatitis Some morbilliform reactions Severe exfoliative dermatoses (eg, SJS/TEN) AGEP DRESS/DiHS Interstitial nephritis Drug-induced hepatitis Other presentations |
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