Antibodies against cellular or matrix antigens cause diseases that specifically affect the cells or tissues where these antigens are present, and these diseases are often not systemic. Antibodies against tissue antigens cause disease by three main mechanisms (Fig. 18-2).
• Antibodies that bind to cell surface antigens may directly opsonize cells, or they may activate the complement system, resulting in the production of complement proteins that opsonize cells. These opsonized cells are phagocytosed and destroyed by phagocytes that express receptors for the Fc portions of IgG antibodies and receptors for complement proteins. This is the principal mechanism of cell destruction in autoimmune hemolytic anemia and autoimmune thrombocy-topenic purpura. The same mechanism is responsible for hemolysis in transfusion reactions (see Chapter 16).
• Antibodies deposited in tissues recruit neutrophils and macrophages, which bind to the antibodies or to attached complement proteins by IgG Fc and complement receptors. These leukocytes are activated by signaling from the receptors, particularly Fc receptors, and leukocyte products, including lysosomal enzymes and reactive oxygen species, are secreted and cause tissue injury. The mechanism of injury in antibody-mediated glomerulonephritis and many other diseases is inflammation and leukocyte activation.
• Antibodies that bind to normal cellular receptors or other proteins may interfere with the functions of these receptors or proteins and cause disease without inflammation or tissue damage. Antibody-mediated functional abnormalities are the cause of Graves' disease and myasthenia gravis.
Antibodies that cause cell- or tissue-specific diseases are usually autoantibodies produced as part of an autoimmune reaction against antigens in these cells or tissues.
Examples of these autoantibodies are listed in Table 18-2. Less commonly, the antibodies may be produced against a foreign (e.g., microbial) antigen that is immunologically cross-reactive with a component of self tissues. In a rare sequel of streptococcal infection called rheumatic fever, antibodies produced against the bacteria cross-react with antigens in the heart, deposit in this organ, and cause inflammation and tissue damage. Tissue deposits of antibodies may be detected by morphologic examination in some of these diseases, and the deposition of antibody is often associated with local complement activation, inflammation, and tissue injury (Fig. 18-3A).
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