CCR6 Regulates the Migration of Inflammatory and Regulatory T Cells
| Autor: | Xuexian O. Yang, Suzanne Craig, Athanasia D. Panopoulos, Bhanu P. Pappu, Hong Soon Kang, Yeonseok Chung, Tomohide Yamazaki, Chen Dong, Li Ma, Qiang Tian, Atsushi Fukunaga, Natalia Martin-Orozco, Anton M. Jetten, Stephanie S. Watowich, Roza Nurieva |
|---|---|
| Rok vydání: | 2008 |
| Předmět: |
Receptors
CCR6 Encephalomyelitis Autoimmune Experimental T cell Molecular Sequence Data Immunology Mice Transgenic chemical and pharmacologic phenomena C-C chemokine receptor type 6 Biology T-Lymphocytes Regulatory Article Mice medicine Animals Immunology and Allergy Amino Acid Sequence STAT3 Cells Cultured Mice Knockout Interleukin-17 Experimental autoimmune encephalomyelitis hemic and immune systems Cell Migration Inhibition Cell migration medicine.disease Cell biology Mice Inbred C57BL CCL20 Chemotaxis Leukocyte medicine.anatomical_structure biology.protein Female Interleukin 17 Inflammation Mediators |
| Zdroj: | Scopus-Elsevier |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.181.12.8391 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|