Gell and Coombs described four types of hypersensitivity reactions:
Type I: Mast cells bind IgE via their Fc(ε) receptors. If subsequently an allergen, by binding to two IgE molecules cross-links the Fc(ε) receptors, the mast cell degranulates and releases mediators that produce allergic reactions. Hypersensitivity usually appears on repeated contact with the allergen.
Type II: Antibody (IgG or IgM) is directed against antigen on an individual's own cells, or against foreign antibody, such as that acquired after blood transfusion. This may lead to cytotoxic action by killer cells, or to lysis mediated by the complement system.
Type III: Immune complexes (antigen and usually IgG or IgM) are deposited in the tissue. Complement is activated and polymorphonuclear cells (to a lesser extent monocytes) are attracted, causing local tissue damage and inflammation. The types of disease encountered are classified into acute and chronic serum sickness, and the Arthus reaction.
Type IV: T cells, sensitized to antigen, release lymphokines following secondary contact with the antigen. Cytokines induce an inflammatory response, they also activate and attract macrophages, which release inflammatory mediators. Antibodies produced against fixed cellular or tissue antigens are usually autoantibodies; less frequently they are produced against extrinsic antigens. Various forms of type IV hypersensitivity (also called delayed hypersensitivity) are recognized: contact hypersensitivity, tuberculin-type hypersensitivity, and granulomatous hypersensitivity.