| First Author | Yuan Q | Year | 2007 |
| Journal | J Exp Med | Volume | 204 |
| Issue | 6 | Pages | 1327-34 |
| PubMed ID | 17548518 | Mgi Jnum | J:125857 |
| Mgi Id | MGI:3760045 | Doi | 10.1084/jem.20062076 |
| Citation | Yuan Q, et al. (2007) CCR4-dependent regulatory T cell function in inflammatory bowel disease. J Exp Med 204(6):1327-34 |
| abstractText | Inflammatory bowel disease (IBD) is an idiopathic inflammatory disease of the intestine. CD4(+) T lymphocytes play an important role in both initiating and regulating intestinal inflammatory immune responses. CD4(+)CD25(+)CD45RB(low) regulatory T (T reg) cells are capable of preventing the development of colitis in a mouse model of IBD. The precise mechanism of T reg cell-mediated prevention of colitis in this model is unclear, and the role of chemokine receptors in the trafficking and function of T reg cells in this model has not been determined. We examined the role of the chemokine receptor CCR4 in in vivo trafficking and suppressive function of T reg cells in a mouse adoptive transfer model of IBD. CCR4-deficient T reg cells failed to accumulate in the mesenteric lymph nodes (MLNs) at early time points (2-5 d) after adoptive transfer, resulting in a failure to suppress the generation of pathogenic T cells and the development of colitis. Moreover, although CCR4-deficent T cells had equivalent in vitro suppressive activity and accumulated in MLNs at later time points (42-56 d), they were unable to suppress colitis. Our study demonstrates that CCR4 plays an important role in T reg cell trafficking in LNs and that this is critical for T reg cell suppressive function in vivo. |
