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  • Title: Cytokine-regulated expression and inhibitory function of FcgammaRIIB1 and -B2 receptors in human dendritic cells.
    Author: Guriec N, Daniel C, Le Ster K, Hardy E, Berthou C.
    Journal: J Leukoc Biol; 2006 Jan; 79(1):59-70. PubMed ID: 16244114.
    Abstract:
    Dendritic cells (DC) capture immune complexes (IC) via Fc receptors for immunoglobulin G FcgammaRII and elicit antigen presentation and protective antitumoral immune response in mice. Two protocols are commonly used to differentiate human monocyte-derived DC in vitro. They associate granulocyte macrophage-colony stimulating factor (CM-CSF) with interleukin (IL)-4 or IL-13. In this study, we first assessed the ability of the two types of DC to initiate an immune response against an IC-linked antigen. We evidenced that IL-4 and IL-13 DC display comparable lymphocyte stimulatory capacity and similar lifetimes. We next characterized FcgammaRIIs expressed by pure populations of circulating myeloid DC (BDCA1+DC), IL-4, and IL-13 DC. We highlighted the expression of FcgammaRIIA, -B1, and -B2 by pure populations of BDCA1 myeloid DCs and IL-4 and IL-13 DC. Moreover, IL-4 and IL-13 DC displayed greater FcgammaRIIB expression than monocytes but a comparable FcgammaRIIA. We next investigated the FcgammaRIIB mechanism of action. We evidenced that deleting FcgammaRIIB increased the ability of IC-pulsed DC to stimulate autologous lymphocytes. FcgammaRIIB acted by lowering IC uptake, surface expression of costimulation molecules, and cytokine release. Finally, the balance between activating FcgammaRIIA/inhibitory FcgammaRIIB (B1+B2) could be modulated in vitro by inflammation mediators. By lowering FcgammaRIIB expression without significantly affecting FcgammaRIIA, prostaglandin E2 (PGE-2) appeared to be a major regulator of this balance. IL-1beta and tumor necrosis factor alpha were also found to potentiate PGE-2 action. Altogether, our results evidence an inhibitory role for FcgammaRIIB in human DC and provide an easy way to possibly improve in vitro the induction of immune response against IC-linked antigen.
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