Circulating phagocytes respond to cytokines and other agents of inflammation by expressing membrane receptors appropriate to the state of immune activation. The stimulus-dependent expression of opsonin receptors is required for effective phagocyte-endothelial contact, diapedesis, migration through the interstitial space, phagocyte- microbe contact recognition, degranulation, and activation of redox metabolism directed to the generation of microbicidal oxidants. The leukocyte integrins (CD! 8 family) and the selectins are necessary for proper adhesion to endothelium and for diapedesis. Mac-1 (CR3; CD11b-CD18) also plays an important role in the activation of respiratory burst metabolism. The complement opsonins C3b and C4b are recognized by CR1 (CD35). IgG opsonins are recognized via the immunoglobulin receptors Fc receptor II (CD32), Fc receptor III (CD16), and under certain conditions, Fc receptor I (CD64). In addition, lipopolysaccharide-binding protein, an opsonin for lipopolysaccharide, is recognized by its membrane receptor (CD14). Large increases in CD11b-CD18, CD35, and CD14 expression follow phagocyte exposure to inflammatory agents. Phagocytosis of IgG-opsonized microbes is also increased by exposure to these agents. The opsonin receptor expression of the circulating phagocyte gauges in vivo exposure to inflammatory agents, and as such, reflects the in vivo state of inflammation. A luminescence method for rapid opsonin receptor analysis of blood phagocytes is described, and an example illustrating the potential use of this methodology in patient diagnosis and management is presented.
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Allen et al. (1992) studied this question.