Which type of hypersensitivity reactions is seen in myasthenia gravis

Ref Robbins 8/e p203;9/e p 206 Antibodies cause disease by targeting cells for phagocyto- sis, by activating the complement system, and by interfer- ing with normal cellular functions (Fig. 4-10). The antibodies that are responsible typically are high-affinity antibodies capable of activating complement and binding to the Fc receptors of phagocytes. * Opsonization and phagocytosis. When circulating cells, such as erythrocytes or platelets, are coated (opsonized) with autoantibodies, with or without complement pro- teins, the cells become targets for phagocytosis by neutrophils and macrophages (Fig. 4-10, A). These phagocytes express receptors for the Fc tails of IgG anti- bodies and for breakdown products of the C3 comple- ment protein, and use these receptors to bind and ingest opsonized paicles. Opsonized cells are usually elimi- nated in the spleen, and this is why splenectomy is ofclinical benefit in autoimmune thrombocytopenia and some forms of autoimmune hemolytic anemia. * Inflammation. Antibodies bound to cellular or tissue anti- gens activate the complement system by the "classical" pathway (Fig. 4-10, B). Products of complement activa- tion serve several functions (see Fig. 2-18, Chapter 2), one of which is to recruit neutrophils and monocytes, triggering inflammation in tissues. Leukocytes may also be activated by engagement of Fc receptors, which rec- ognize the bound antibodies. This mechanism of injury is exemplified by Goodpasture syndrome and pemphi- gus vulgaris. * Antibody-mediated cellular dysfunction. In some cases, antibodies directed against cell surface receptors impair or dysregulate cellular function without causing cell injury or inflammation (Fig. 4-10, C). In myasthenia gravis, antibodies against acetylcholine receptors in the motor end plates of skeletal muscles inhibit neuromuscular transmission, with resultant muscle weakness. Antibodies can also stimulate cellularresponses excessively. In Graves disease, antibodies against the thyroid-stimulating hormone receptor stim- ulate thyroid epithelial cells to secrete thyroid hormones, resulting in hypehyroidism. Antibodies against hor- mones and other essential proteins can neutralize and block the actions of these molecules, causing functional derangements.