Rh incomatibility is-
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 exogenous antigens (e.g., a drug metabolite). Antibody-mediated abnormalities are the underlying cause of many human diseases; . In all of these disorders, the tissue damage or functional abnormalities result from a limited number of mechanisms. Mechanisms of Antibody-Mediated Diseases Antibodies cause disease by targeting cells for phagocytosis, by activating the complement system, and by interfering with normal cellular functions . 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 proteins, the cells become targets for phagocytosis by neutrophils and macrophages . These phagocytes express receptors for the Fc tails of IgG antibodies and for breakdown products of the C3 complement protein, and use these receptors to bind and ingest opsonized paicles. Opsonized cells are usually eliminated in the spleen, and this is why splenectomy is of 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 Products of complement activa-tion serve several functions , 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 . 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 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. Robbins 9 th edition page no. 114
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hyperseninsitivity
General pathology