Suppression of autoimmune inflammation of the central nervous system by interleukin 10 secreted by interleukin 27-stimulated T cells

Nat Immunol. 2007 Dec;8(12):1372-9. doi: 10.1038/ni1540. Epub 2007 Nov 11.


Excessive inflammation occurs during infection and autoimmunity in mice lacking the alpha-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-gamma and expressed the transcription factor T-bet but did not express the transcription factor Foxp3. These IFN-gamma+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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Autoimmunity / drug effects*
  • Autoimmunity / immunology
  • Central Nervous System Diseases / immunology
  • Central Nervous System Diseases / pathology
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Inflammation / immunology
  • Interleukin-10 / immunology
  • Interleukin-10 / metabolism*
  • Interleukin-17 / immunology*
  • Interleukin-17 / pharmacology
  • Lymphocyte Activation / drug effects
  • Lymphocyte Activation / immunology
  • Mice
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism*
  • T-Lymphocytes, Regulatory / immunology*


  • Interleukin-17
  • Interleukin-10