The Journal of Experimental Medicine
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Published online June 4, 2007
doi:10.1084/jem.20062076
The Journal of Experimental Medicine, Vol. 204, No. 6, 1327-1334
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Yuan et al.
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BRIEF DEFINITIVE REPORT

 CCR4-dependent regulatory T cell function in inflammatory bowel disease

Qian Yuan1,2, Shannon K. Bromley1, Terry K. Means1, Krister J. Jones1,2, Fumitaka Hayashi1, Atul K. Bhan3, and Andrew D. Luster1

1 Division of Rheumatology, Allergy and Immunology, Center for Immunology and Inflammatory Diseases; 2 Division of Pediatric Gastroenterology and Nutrition, Department of Pediatrics; and 3 Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114

CORRESPONDENCE Andrew D. Luster: luster.andrew{at}mgh.harvard.edu

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+CD45RBlow 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.


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