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A correction to this article has been published: Dhodapkar et al., J. Exp. Med. 204 (10) 2489
A correction to this article has been published: Dhodapkar et al., J. Exp. Med. 204 (10) 2494
Published online
doi:10.1084/jem.20062545
The Journal of Experimental Medicine, Vol. 204, No. 6, 1359-1369
The Rockefeller University Press, 0022-1007 $30.00
© Dhodapkar et al.
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ARTICLE

Selective blockade of the inhibitory Fc{gamma} receptor (Fc{gamma}RIIB) in human dendritic cells and monocytes induces a type I interferon response program

Kavita M. Dhodapkar1, Devi Banerjee1, John Connolly6, Anjli Kukreja3, Elyana Matayeva1, Maria Concetta Veri5, Jeffrey V. Ravetch2,4, Ralph M. Steinman1,4, and Madhav V. Dhodapkar3,4

1 Lab of Cellular Physiology and Immunology, 2 Lab of Molecular Genetics and Immunology, 3 Lab of Tumor Immunology and Immunotherapy, and 4 Chris Browne Center for Immunology, The Rockefeller University, New York, NY 10021
5 MacroGenics, Inc., Rockville, MD 20850
6 Baylor Institute of Immunology Research, Dallas, TX 75204

CORRESPONDENCE Kavita M. Dhodapkar: dhodapk{at}rockefeller.edu

The ability of dendritic cells (DCs) to activate immunity is linked to their maturation status. In prior studies, we have shown that selective antibody-mediated blockade of inhibitory Fc{gamma}RIIB receptor on human DCs in the presence of activating immunoglobulin (Ig) ligands leads to DC maturation and enhanced immunity to antibody-coated tumor cells. We show that Fc{gamma} receptor (Fc{gamma}R)–mediated activation of human monocytes and monocyte-derived DCs is associated with a distinct gene expression pattern, including several inflammation-associated chemokines, as well as type 1 interferon (IFN) response genes, including the activation of signal transducer and activator of transcription 1 (STAT1). Fc{gamma}R-mediated STAT1 activation is rapid and requires activating Fc{gamma}Rs. However, this IFN response is observed without a detectable increase in the expression of type I IFNs themselves or the need to add exogenous IFNs. Induction of IFN response genes plays an important role in Fc{gamma}R-mediated effects on DCs, as suppression of STAT1 by RNA interference inhibited Fc{gamma}R-mediated DC maturation. These data suggest that the balance of activating/inhibitory Fc{gamma}Rs may regulate IFN signaling in myeloid cells. Manipulation of Fc{gamma}R balance on DCs and monocytes may provide a novel approach to regulating IFN-mediated pathways in autoimmunity and human cancer.


Abbreviations used: Fc{gamma}R, Fc{gamma} receptor; GEP, gene expression profile; IC, immune complex; IDC, immature DC; IFI, IFN-{alpha} inducible; IFNAR, IFN-{alpha} receptor; IRG, IFN response gene; STAT, signal transducer and activator of transcription.


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