| First Author | Fitzgerald DC | Year | 2007 |
| Journal | Nat Immunol | Volume | 8 |
| Issue | 12 | Pages | 1372-9 |
| PubMed ID | 17994023 | Mgi Jnum | J:127773 |
| Mgi Id | MGI:3764796 | Doi | 10.1038/ni1540 |
| Citation | Fitzgerald DC, et al. (2007) Suppression of autoimmune inflammation of the central nervous system by interleukin 10 secreted by interleukin 27-stimulated T cells. Nat Immunol 8(12):1372-9 |
| abstractText | 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. |
