Journal of Leukocyte Biology
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Originally published online as doi:10.1189/jlb.0305155 on October 21, 2005

Published online before print October 21, 2005
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(Journal of Leukocyte Biology. 2006;79:59-70.)
© 2006 by Society for Leukocyte Biology

Cytokine-regulated expression and inhibitory function of Fc{gamma}RIIB1 and -B2 receptors in human dendritic cells

Nathalie Guriec1, Catherine Daniel2, Karine Le Ster, Elisabeth Hardy and Christian Berthou

Brest Medical School, Cellular Therapy Laboratory, France

1 Correspondence: Brest Medical School, Cellular Therapy Laboratory, 22, avenue Camille Desmoulins, 29200 Brest, France. E-mail: nguriec{at}voila.fr

Dendritic cells (DC) capture immune complexes (IC) via Fc receptors for immunoglobulin G Fc{gamma}RII 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 Fc{gamma}RIIs expressed by pure populations of circulating myeloid DC (BDCA1+DC), IL-4, and IL-13 DC. We highlighted the expression of Fc{gamma}RIIA, -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 Fc{gamma}RIIB expression than monocytes but a comparable Fc{gamma}RIIA. We next investigated the Fc{gamma}RIIB mechanism of action. We evidenced that deleting Fc{gamma}RIIB increased the ability of IC-pulsed DC to stimulate autologous lymphocytes. Fc{gamma}RIIB acted by lowering IC uptake, surface expression of costimulation molecules, and cytokine release. Finally, the balance between activating Fc{gamma}RIIA/inhibitory Fc{gamma}RIIB (B1+B2) could be modulated in vitro by inflammation mediators. By lowering Fc{gamma}RIIB expression without significantly affecting Fc{gamma}RIIA, prostaglandin E2 (PGE-2) appeared to be a major regulator of this balance. IL-1ß and tumor necrosis factor {alpha} were also found to potentiate PGE-2 action. Altogether, our results evidence an inhibitory role for Fc{gamma}RIIB in human DC and provide an easy way to possibly improve in vitro the induction of immune response against IC-linked antigen.

Key Words: phagocytes • immunotherapy • inflammation • immunoglobulin • antigen presentation






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