Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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A more recent version of this article appeared on January 1, 2006

Published online before print October 21, 2005
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0305155

Received for publication March 18, 2005.
Revised July 19, 2005.
Accepted for publication August 9, 2005.

Article

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

Nathalie Guriec @, Catherine Daniel , Karine Le Ster , Elisabeth Hardy , and Christian Berthou

Brest Medical School, Cellular Therapy Laboratory, France

@ To whom correspondence should be addressed. E-mail: nguriec{at}voila.fr.


  Abstract

Dendritic cells (DCs) capture immune complexes (ICs) via Fc receptors for immunoglobulin G (Fc{gamma}R)II and elicit antigen presentation and protective antitumoral immune response in mice. Two protocols are commonly used to differentiate human monocyte-derived DCs in vitro. They associate granulocyte macrophage-colony stimulating factor with interleukin (IL)-4 or IL-13. In this study, we first assessed the ability of the two types of DCs to initiate an immune response against an IC-linked antigen. We evidenced that IL-4 and IL-13 DCs display comparable lymphocyte stimulatory capacity and similar lifetimes. We next characterized Fc{gamma}RIIs expressed by pure populations of circulating myeloid DCs, IL-4, and IL-13 DCs. We highlighted the expression of Fc{gamma}RIIA, -B1, and -B2 by pure populations of circulating blood DC antigen-1+ myeloid DCs and IL-4 and IL-13 DCs. Moreover, IL-4 and IL-13 DCs 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 DCs 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-1{beta} 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 DCs 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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Copyright © 2005 by the Society for Leukocyte Biology.