Activation of Macrophage Complement Receptors for Phagocytosis
Engagement by immunoglobulin G (IgG) of Fc receptors of either polymorphonuclear or mononuclear phagocytes virtually always leads to ingestion of IgG-containing soluble and particulate complexes (Bianco et al., 1975; Ehlenberger and Nussenzweig, 1977; F. M. Griffin etal., 1975b, 1976; J. A. Griffin and Griffin, 1979; Mantovani, 1975; Mantovani et al., 1972;Quie et a1.,1968; Rabinovitch, 1967; Schreiber and Frank, 1972; Shaw and Griffin, 1981). Engagement of C3b receptors* by C3b contained in soluble immune complexes likewise results in ingestion of the complexes (Van Snick and Masson, 1978). A number of studies (Bar-Shavit et al., 1979; Diamond et al., 1973, 1974; Gigli and Nelson, 1968; Horwitz and Silverstein, 1980; Huber et al., 1968; Musson and Becker, 1977; Pearlman et al., 1969; Schreiber et al., 1982; Shurin and Stossel, 1978; Stossel et al., 1973) have demonstrated enhancement of phagocytosis of a variety of particles, chiefly microoraganisms, when they were coated with complement, even in the absence of immunoglobulin, and for many years it was assumed that ingestion of these microbes was mediated by the complement receptors of phagocytic cells. Several recent studies, however, have reported that engagement by particle-bound C3b of complement receptors of neutrophils, monocytes, and “resting” tissue macrophages, although always promoting efficient particle binding, fails to promote ingestion of C3b-coated particles (Bianco et al., 1975; Ehlenberger and Nussenzweig, 1977; F. M. Griffin, 1980,1981; F. M. Griffin et al.,1975a,b; F. M. Griffin and Griffin, 1980; J. A. Griffin and Griffin, 1979; Lay and Nussenzweig, 1968; Mantovani, 1975; Mantovani et al.,1972; Newman and Johnston, 1979; Scribner and Fahrney, 1976; Shaw and Griffin, 1981; Ward and Enders, 1933). Studies in rabbits (Brown et al., 1970) and guinea pigs Atkinson and Frank, 1974a,b; Schreiber and Frank, 1972) confirm the in vitro finding that macrophages are normally unable to phagocytize via their complement receptors. Erythrocytes coated with IgM, which became further coated with complement when injected intravenously, were rapidly cleared from these animals’ circulation by the liver. However, within a few minutes they reappeared in the bloodstream and circulated with a normal lifespan. Presumably these C3b-coated erythrocytes were bound via the C3b receptors of Kupffer cells but were released when C3b inactivator and proteases cleaved erythrocyte-bound C3b to C3 fragments not recognized by macrophages.
KeywordsComplement Receptor Mouse Peritoneal Macrophage Receptor Mobility Thioglycollate Medium Soluble Immune Complex
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