Journal
JOURNAL OF IMMUNOLOGY
Volume 181, Issue 12, Pages 8391-8401Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.12.8391
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Funding
- National Institutes of Health
- National Institute on Environmental Health Sciences
- Leukemia and Lymphoma Society
- Anderson Cancer Center
- Gillson Longenbaugh Foundation
- Odyssey Program
- Kimberly-Clark Foundation Award for Scientific Achievement at MD Anderson Cancer Center
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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-beta and requires two nuclear receptors, ROR alpha and ROR gamma. Th17 cells also express the CCR6 ligand CCL20, which is induced synergistically by TGF-beta and IL-6, which requires STAT3, ROR gamma 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 Journal of Immunology, 2008, 181: 8391-8401.
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