Type II Autoimmune Reactions - Mechanisms of Autoimmune Tissue Injury and Examples

 MECHANISMS OF AUTOIMMUNE TISSUE INJURY AND EXAMPLES

Tissue damage in autoimmune diseases can occur through several mechanisms, which are analogous to three of the classical types of hypersensitivity reactions: type II (caused by autoantibodies reactive with cell surface or matrix antigens), type III (caused by immune complexes), and type IV (delayed-type hypersensitivity, mediated by T cells).

 

Type II Autoimmune Reactions

Type II hypersensitivity reactions are caused by antibodies against altered self-proteins, such as penicillin–protein conjugates. In the case of autoimmunity, antibodies generated against cell surface antigens/extracellular matrix proteins may be cytotoxic (type IIA) or they may have agonistic/antagonistic properties (type IIB). Autoantibodies to cell surface anti-gens may initiate cell destruction by com-plement-mediated lysis (cell destruction), phagocytosis, or antibody-dependent cell-mediated cytotoxicity (ADCC).

Examples include autoimmune hemolytic anemia (AIHA), and autoimmune throm-bocytopenia (Table 6.1). Some autoanti-bodies bind to surface receptors, either activating (e.g., anti-TSH receptor auto-antibodies in Graves’ disease) or inhibit-ing (e.g., anti-acetylcholine antibodies in myasthenia gravis) their function.


Table 6.1 Some Human Autoimmune Diseases



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