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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