CCR6 Regulates the Migration of Inflammatory and Regulatory T Cells

被引：417

作者：

Yamazaki, Tomohide ^{[1
]}

Yang, Xuexian O. ^{[1
]}

Chung, Yeonseok ^{[1
]}

Fukunaga, Atsushi ^{[1
]}

Nurieva, Roza ^{[1
]}

Pappu, Bhanu ^{[1
]}

Martin-Orozco, Natalia ^{[1
]}

Kang, Hong Soon ^{[2
]}

Ma, Li ^{[3
]}

Panopoulos, Athanasia D. ^{[1
]}

Craig, Suzanne

Watowich, Stephanie S. ^{[1
]}

Jetten, Anton M. ^{[2
]}

Tian, Qiang ^{[3
]}

Dong, Chen ^{[1
]}

机构：

[1] Univ Texas Houston, MD Anderson Canc Ctr, Dept Immunol, Houston, TX 77030 USA

[2] Natl Inst Environm Sci, Cell Biol Sect, Lab Resp Biol, NIH, Res Triangle Pk, NC 27709 USA

[3] Inst Syst Biol, Seattle, WA 98103 USA

来源：

JOURNAL OF IMMUNOLOGY | 2008年 / 181卷 / 12期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.4049/jimmunol.181.12.8391

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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.

引用

页码：8391 / 8401

页数：11

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