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* Department of Immunology,
Veterinary Medicine & Surgery, M.D. Anderson Cancer Center, Houston, TX 77030;
Cell Biology Section, Laboratory of Respiratory Biology, National Institute on Environmental Sciences, National Institutes of Health, Research Triangle Park, NC 27709; and
Institute for Systems Biology, Seattle, WA 98103
Th17 and regulatory T (Treg) cells play opposite roles in autoimmune diseases. However, the mechanisms underlying their proper migration to inflammatory tissues are unclear. In this study, we report that these two T cell subsets both express CCR6. CCR6 expression in Th17 cells is regulated by TGF-β and requires two nuclear receptors, ROR
and ROR
. Th17 cells also express the CCR6 ligand CCL20, which is induced synergistically by TGF-β and IL-6, which requires STAT3, ROR and IL-21. Th17 cells, by producing CCL20, promote migration of Th17 and Treg cells in vitro in a CCR6-dependent manner. Lack of CCR6 in Th17 cells reduces the severity of experimental autoimmune encephalomyelitis and Th17 and Treg recruitment into inflammatory tissues. Similarly, CCR6 on Treg cells is also important for their recruitment into inflammatory tissues. Our data indicate an important role of CCR6 in Treg and Th17 cell migration.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by research grants from the National Institutes of Health (to C.D.), an Intramural Research Program of the National Institute on Environmental Health Sciences, National Institutes of Health (to A.M.J.), the Leukemia and Lymphoma Society (to C.D.) and M.D. Anderson Cancer Center (to C.D. and S.S.W.), and the Gillson Longenbaugh Foundation (to S.S.W.). T.Y. received a fellowship from the Odyssey Program and The Kimberly-Clark Foundation Award for Scientific Achievement at MD Anderson Cancer Center. R.N. is a recipient of a Scientist Development Grant from the American Heart Association. C.D. is a Trust Fellow of the MD Anderson Cancer Center, a Cancer Research Institute Investigator, a Leukemia and Lymphoma Society Scholar, and an American Lung Association Career Investigator.
2 Address correspondence and reprint requests to Dr. Chen Dong, Department of Immunology and Center for Cancer Immunology Research, University of Texas M.D. Anderson Cancer Center, Houston, TX 77030. E-mail address: cdong{at}mdanderson.org
3 Abbreviations used in this paper: EAE, experimental autoimmune encephalomyelitis; nTreg, natural regulatory T; Treg, regulatory T; iTreg, inducible Treg; KO, knockout; BM, bone marrow; MOG, myelin oligodendrocyte glycoprotein; LN, lymph node; WT, wild type.
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  G. E. Katsifis, S. Rekka, N. M. Moutsopoulos, S. Pillemer, and S. M. Wahl Systemic and Local Interleukin-17 and Linked Cytokines Associated with Sjogren's Syndrome Immunopathogenesis Am. J. Pathol., September 1, 2009; 175(3): 1167 - 1177. [Abstract] [Full Text] [PDF]
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