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- Publisher
- Springer Journals
- Copyright
- Copyright © 2007 by Nature Publishing Group
- Subject
- Biomedicine; Biomedicine, general; Immunology; Infectious Diseases
- ISSN
- 1529-2908
- eISSN
- 1529-2916
- DOI
- 10.1038/ni1540
- Publisher site
- See Article on Publisher Site
Abstract
Excessive inflammation occurs during infection and autoimmunity in mice lacking the α-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-γ and expressed the transcription factor T-bet but did not express the transcription factor Foxp3. These IFN-γ+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.
Journal
Nature Immunology – Springer Journals
Published: Nov 11, 2007