NDLI: Cutting Edge: IL-27 Attenuates Autoimmune Neuroinflammation via Regulatory T Cell/Lag3–Dependent but IL-10

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Cutting Edge: IL-27 Attenuates Autoimmune Neuroinflammation via Regulatory T Cell/Lag3–Dependent but IL-10–Independent Mechanisms In Vivo

Content Provider	Scilit
Author	Kim, DongKyun Le, Hongnga T. Nguyen, Quang Tam Kim, Sohee Lee, Juyeun Min, Booki
Copyright Year	2019
Description	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-27Rα 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.
Ending Page	1685
Page Count	6
Starting Page	1680
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1800898
Alternate Webpage(s)	https://www.jimmunol.org/content/jimmunol/202/6/1680.full.pdf
Journal	The Journal of Immunology
Issue Number	6
Volume Number	202
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2019-03-15
Access Restriction	Open
Subject Keyword	Cd4 T Cells
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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