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Part of the book series: Immunology and Medicine Series ((IMME,volume 26))

Abstract

This chapter focuses on the Fc receptors for IgG (FcγR) on phagocytic cells, e.g. polymorphonuclear neutrophils (PMNs), monocytes and macrophages. Eosinophils and basophils/mast cells which also have phagocytic properties are not discussed. PMNs and monocytes circulate in the bloodstream and are derived from pluripotent haematopoietic stem cells in the bone marrow. Macrophages are derived from blood-borne monocytes and together with PMNs are found in tissues. The ingestion of antibody-coated microorganisms and cells is one of the important immunological functions of PMNs, monocytes and macrophages. The identity of the Fcγreceptors on these phagocytes, the ligand binding and signal transducing subunits, the patterns and control of expression and the immediate and downstream signals in phagocyte activation will be discussed. The Fc receptors for IgG on phagocytes belong to 3 classes: FcγRI (CD64), FcγRII (CD32) and FcγRIII (CD16), distinguishable by size and structure, gene origin and reactivity with anti-FcγR monoclonal antibodies. The cellular pattern of expression, the structure, and the subunits for the 3 classes of FcγR on phagocytes are summarized in Figure 9.1. Of the FcγRI genes, the FcγRIA gene is responsible for the expression of the known FcγRI protein. FcγRIIIA is expressed on monocytes/macrophages and FcγRIIIB is expressed on PMNs. The three FcγRII genes encode FcγRIIA, FcγRIIB and FcγRIIC. FcγRI and FcγRIIIA physically associate with γchain homodimers which constitute the signal transducing subunit for the ligand-binding subunits. In contrast, FcγRIIA mediates signals in the absence of associated subunits through sequences within its own cytoplasmic domain (see below).

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Mckenzie, S.E., Indik, Z.K., Schreiber, A.D. (1998). Phagocyte Fc receptors for IgG. In: van de Winkel, J.G.J., Hogarth, P.M. (eds) The Immunoglobulin Receptors and their Physiological and Pathological Roles in Immunity. Immunology and Medicine Series, vol 26. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-5018-7_9

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