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* Department of Molecular Biology, Genentech, Inc., South San Francisco, CA 94080; and
Washington University School of Medicine, Pulmonary and Critical Care Medicine, St. Louis, MO 63110
The cytokine IL-27 is important for restricting inflammation in response to a wide variety of immune challenges. In this study, we demonstrate that IL-27 induces expression of the anti-inflammatory cytokine IL-10 by CD4+ and CD8+ T cells. IL-27 relied upon the Th1 transcription factor STAT1 to induce IL-10+IFN-
+FoxP3– Th1 cells, which were recently shown to be key negative regulators during certain infections. Il27ra–/– mice generated fewer IL-10+ T cells during both Listeria monocytogenes infection and experimental autoimmune encephalomyelitis. The data presented here indicate a novel mechanism for the induction of IL-10 expression by T cells and provide a mechanistic basis for the suppressive effects of IL-27.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 Address correspondence and reprint requests to Dr. Nico Ghilardi, Department of Molecular Biology, Genentech, Inc., 1 DNA Way, MS37, South San Francisco, CA 94080. E-mail address: ghilardi{at}gene.com
2 Abbreviations used in this paper: Ebi3, EBV-induced protein 3; EAE, experimental immune encephalomyelitis; m, murine; MOG, myelin oligodendrocyte glycoprotein; rh, recombinant human; rm, recombinant murine; Treg, regulatory T cell.
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