| First Author | Kitamura K | Year | 2010 |
| Journal | J Immunol | Volume | 185 |
| Issue | 6 | Pages | 3295-304 |
| PubMed ID | 20720211 | Mgi Jnum | J:163538 |
| Mgi Id | MGI:4822276 | Doi | 10.4049/jimmunol.1001156 |
| Citation | Kitamura K, et al. (2010) CCR6 Marks Regulatory T Cells as a Colon-Tropic, IL-10-Producing Phenotype. J Immunol 185(6):3295-304 |
| abstractText | Expression of CCR6 and its ligand, CCL20, are increased in the colon of humans with inflammatory bowel diseases and mice with experimental colitis; however, their role in disease pathogenesis remains obscure. In this study, we demonstrate a role for CCR6 on regulatory T (Treg) cells in the T cell-transfer model of colitis. Rag2(-/-) mice given Ccr6(-/-)CD4(+)CD45RB(high) T cells had more severe colitis with increased IFN-gamma-producing T cells, compared with the mice given wild-type cells. Although an equivalent frequency of induced/acquired Treg (iTreg) cells was observed in mesenteric lymph nodes and colon from both groups, the suppressive capacity of Ccr6(-/-) iTreg cells was impaired. Cotransfer studies of wild-type or Ccr6(-/-) Treg cells with CD4(+)CD45RB(high) T cells also showed a defect in suppression by Ccr6(-/-) Treg cells. CCR6(+) Treg cells were characterized as Ag-activated and IL-10-producing in the steady-state and preferentially migrated to the colon during inflammation. Thus, we conclude that CCR6 expression on Treg cells was required for the full function of Treg cell-mediated suppression in the T cell-transfer model of colitis. CCR6 may contribute to the regulation of colitis by directing its function in Ag-specific, IL-10-producing iTreg cells to the inflamed colon. |
