Article abstract
Nature Immunology 8, 1372 - 1379 (2007)
Published online: 11 November 2007 | Corrected online: 28 November 2007 | doi:10.1038/ni1540
There is a Corrigendum (January 2008) associated with this Article.
Suppression of autoimmune inflammation of the central nervous system by interleukin 10 secreted by interleukin 27–stimulated T cells
Denise C Fitzgerald1, Guang-Xian Zhang1, Mohamed El-Behi1, Zoë Fonseca-Kelly1, Hongmei Li1, Shuo Yu1, Christiaan J M Saris2, Bruno Gran1,3, Bogoljub Ciric1 & Abdolmohamad Rostami1
Abstract
Excessive inflammation occurs during infection and autoimmunity in mice lacking the 
-subunit of the interleukin 27 (IL-27) receptor. The molecular mechanisms underlying this increased inflammation are incompletely understood. Here we report that IL-27 upregulated IL-10 in effector T cells that produced interferon-
and expressed the transcription factor T-bet but did not express the transcription factor Foxp3. These IFN-+T-bet+Foxp3- cells resembled effector T cells that have been identified as the main source of host-protective IL-10 during inflammation. IL-27-induced production of IL-10 was associated with less secretion of IL-17, and exogenous IL-27 reduced the severity of adoptively transferred experimental autoimmune encephalomyelitis by a mechanism dependent on IL-10. Our data show that IL-27-induced production of IL-10 by effector T cells contributes to the immunomodulatory function of IL-27.
- Department of Neurology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
- Department of Inflammation Research, Amgen, Thousand Oaks, California 91320, USA.
- Present address: Division of Clinical Neurology, Nottingham University Hospitals, Queen's Medical Centre Campus, Nottingham NG7 2UH, UK.
Correspondence to: Abdolmohamad Rostami1 e-mail: a.m.rostami@jefferson.edu
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