Journal
JOURNAL OF IMMUNOLOGY
Volume 202, Issue 6, Pages 1680-1685Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1800898
Keywords
-
Categories
Funding
- National Multiple Sclerosis Society [RG1411-02051]
- National Institutes of Health [AI125247, AI121524]
Ask authors/readers for more resources
IL-27 regulates immune responses in inflammation. The underlying mechanism of IL-27 functions has long been attributed to its ability to induce IL-10 production in activated CD4 T cells. In this study, we report that Foxp3(+) regulatory T cells (Tregs) are the main target cells of IL-27, mediating its immunoregulatory functions in vivo. Systemically delivered IL-27 efficiently prevents the development of experimental autoimmune encephalomyelitis, an autoimmune inflammation in the CNS. However, it failed to do so upon Treg depletion. IL-27 signaling in Tregs was necessary, as transferring Tregs deficient in IL-27R alpha or Lag3, a downstream molecule induced by IL-27, was unable to protect mice from experimental autoimmune encephalomyelitis. IL-27 efficiently induced IL-10 expression in CD4 T cells in vitro; however, we found no evidence supporting IL-27-induced IL-10 induction in CD4 T cells in vivo Taken together, our results uncover an irreplaceable contribution of Tregs during IL-27-mediated control of inflammation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available