CCR6 regulates the migration of inflammatory and regulatory T cells

Tomohide Yamazaki, Xuexian O. Yang, Yeonseok Chung, Atsushi Fukunaga, Roza Nurieva, Bhanu Pappu, Natalia Martin-Orozco, Hong Soon Kang, Li Ma, Athanasia D. Panopoulos, Suzanne Craig, Stephanie S. Watowich, Anton M. Jetten, Qiang Tian, Chen Dong

Research output: Contribution to journalArticlepeer-review

407 Scopus citations

Abstract

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, RORα and RORγ. Th17 cells also express the CCR6 ligand CCL20, which is induced synergistically by TGF-β and IL-6, which requires STAT3, RORγ 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.

Original languageEnglish (US)
Pages (from-to)8391-8401
Number of pages11
JournalJournal of Immunology
Volume181
Issue number12
DOIs
StatePublished - Dec 15 2008

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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