Example of type 2 hypersensitivity is
Ref Robbins 9/e p206 Antibody-Mediated Diseases (Type II Hypersensitivity) Antibody-mediated (type II) hypersensitivity disorders are caused by antibodies directed against target antigens on the surface of cells or other tissue components. The antigens may be normal molecules intrinsic to cell membranes or in the extracellular matrix, or they may be adsorbed exoge- nous antigens (e.g., a drug metabolite). Antibody-mediated abnormalities are the underlying cause of many human diseases; examples of these are listed in Table 4-3. In all of these disorders, the tissue damage or functional abnormali- ties result from a limited number of mechanisms. Mechanisms of Antibody-Mediated Diseases 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 of Table 4-3 Examples of Antibody-Mediated Diseases (Type II Hypersensitivity) clinical 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 cellular Figure 4-10 Mechanisms of antibody-mediated injury. A, Opsonization of cells by antibodies and complement components, and ingestion of opso- nized cells by phagocytes. B, Inflammation induced by antibody binding to Fc receptors of leukocytes and by complement breakdown products. C, Antireceptor antibodies disturb the normal function of receptors. In these examples, antibodies against the thyroid-stimulating hormone (TSH) receptor activate thyroid cells in Graves disease, and acetylcholine (ACh) receptor antibodies impair neuromuscular transmission in myasthenia g responses 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.
Blood transfusion reaction
Ahur reaction
Hay fever
Post streptococcal glomerulonephritis
General anatomy