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Negative Regulation of Hematopoietic Cell Activation and Proliferation by FcγRIIB

  • Chapter
Immunoreceptor Tyrosine-based Inhibition Motifs

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 244))

Abstract

FcγRIIB are single-chain, low-affinity receptors for the Fc portion of IgG which belong to the immunoglobulin superfamily (Daëron 1997a). They bind IgG antibodies either complexed to multivalent soluble antigens or bound to cell membrane antigens. The FcγRIIB gene possesses three exons that encode the intracytoplasmic domain. By alternative splicing, it generates two (in humans) or three (in mice) isoforms of membrane FcγRIIB that differ only in their intracytoplasmic sequences (Ravetch et al. 1986; Hibbs et al. 1986; Lewis et al. 1986;Brooks et al. 1989; Latour et al. 1996). FcγRIIB are involved in the internalization of IgG immune complexes; and FcγRIIB isoforms were shown to differentially mediate the phagocytosis of particulate immune complexes and/or the endocytosis of soluble immune complexes (Daëron et al. 1993). No FcγRIIB isoform is able to trigger cell activation (Daëron et al. 1992). Instead, all isoforms were found to negatively regulate cell activation.

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  1. Laboratoire d’Immunologie Cellulaire et Clinique, INSERM U.255, Institut Curie, Paris, France

    O. Malbec, W. H. Fridman & M. Daëron

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  1. O. Malbec
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  2. W. H. Fridman
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  3. M. Daëron
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  1. Laboratoire d’Immunologie Cellulaire et Clinique INSERM U.255, Institut Curie, 26 rue d’Ulm, F-75005, Paris, France

    Marc Daëron M.D. Ph.D.

  2. Centre d’Immunologie INSERM-CNRS de Marseille Luminy, Institut Universitaire de France, Parc Scientifique de Luminy-Case 906, F-13288, Marseille Cedex 9, France

    Eric Vivier DUM, Ph.D.

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Malbec, O., Fridman, W.H., Daëron, M. (1999). Negative Regulation of Hematopoietic Cell Activation and Proliferation by FcγRIIB. In: Daëron, M., Vivier, E. (eds) Immunoreceptor Tyrosine-based Inhibition Motifs. Current Topics in Microbiology and Immunology, vol 244. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-58537-1_2

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  • DOI: https://doi.org/10.1007/978-3-642-58537-1_2

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