Journal of Leukocyte Biology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

A more recent version of this article appeared on January 1, 2006

Published online before print October 21, 2005
This Article
Right arrow Full Text (Reprint (PDF))
Right arrow All Versions of this Article:
jlb.0305155v1
79/1/59    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Guriec, N.
Right arrow Articles by Berthou, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Guriec, N.
Right arrow Articles by Berthou, C.
© 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






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2005 by the Society for Leukocyte Biology.