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