An immune complex consists of antigen and antibody bound together, often with some complement components. Immune complexes usually adhere to Fc receptors on cells of the mononuclear phagocyte system and are engulfed and destroyed intracellularly, especially if they are large complexes. Under ordinary circumstances, they are rapidly removed from circulation. In conditions where a moderate excess of antigen over antibody exists, however, the small complexes formed are not quickly removed and destroyed but persist in circulation or at their sites of formation in tissue. Immune complexes possess considerable biological activity. They initiate the blood clotting mechanism, and they activate components of complement that attract neutrophils into the area and contribute to inflammation (figure 18.5). Proteases released from the neutrophils are especially active in inducing tissue damage. Circulating immune complexes are commonly deposited in skin, in joints, and in the kidneys, where they cause glomerulonephritis. Immune complexes are responsible for the rashes, joint pains, and other symptoms seen in a number of diseases, such as farmer's lung, bacterial endocarditis, early rubella infection, and malaria. Immune complexes can also precipitate a devastating condition, disseminated intravascular coagulation, in which clots form in small blood vessels, leading to failure of vital organs. ■ disseminated intravascular coagulation, p. 720 ■ glomerulonephritis, pp. 540, 718
Immune complex disease may arise during a variety of bacterial, viral, and protozoan infections, as well as from inhaled dusts or bacteria and injected medications such as penicillin. The steps in the formation of immune complex pathology are summarized in table 18.3.
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