NDLI: IFN-Î³ limits Th9-mediated autoimmune inflammation through dendritic cell modulation of IL-27.

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IFN-Î³ limits Th9-mediated autoimmune inflammation through dendritic cell modulation of IL-27.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Joller, Nicole Murugaiyan, Gopal Beynon, Vanessa Pires Da Cunha, Andre Weiner, Howard L.
Description	Country affiliation: United States Author Affiliation: Murugaiyan G ( Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.)
Abstract	IL-9-producing Th9 cells have been associated with autoimmune diseases, such as experimental autoimmune encephalitis. However, the factors that negatively regulate Th9 cells during autoimmune inflammation are unclear. In this article, we show that IFN-Î³ inhibits Th9 differentiation both in vitro and in vivo. This suppressive activity was dependent on the transcription factor STAT-1. In addition to its direct inhibitory effect on Th9 differentiation, IFN-Î³ suppressed Th9 cells through the induction of IL-27 from dendritic cells. In vitro, treatment of naive CD4(+) T cells with IL-27 suppressed the development of Th9 cells, which was partially dependent on the transcription factors STAT-1 and T-bet. Moreover, IL-27 treatment completely abrogated the encephalitogenicity of Th9 cells in the experimental autoimmune encephalomyelitis model. Thus, our results identify a previously unknown mechanism by which IFN-Î³ limits Th9-mediated autoimmune inflammation through dendritic cell modulation of IL-27.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1200808
Journal	The Journal of Immunology
Issue Number	11
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Dendritic Cells Drug Effects Encephalomyelitis, Autoimmune, Experimental Drug Therapy Inflammation Interferon-gamma Pharmacology Interleukin-9 Immunology Interleukins T-lymphocytes, Helper-inducer Animals Cell Differentiation Cytology Chemically Induced Complications Gene Expression Interleukin-17 Biosynthesis Mice Mice, Inbred C57bl Mice, Knockout Myelin-oligodendrocyte Glycoprotein Peptide Fragments Stat1 Transcription Factor Genetics Signal Transduction T-box Domain Proteins Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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