The Journal of Experimental Medicine
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Published online June 4, 2007
doi:10.1084/jem.20070081
The Journal of Experimental Medicine, Vol. 204, No. 6, 1335-1347
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Sather et al.
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ARTICLE

 Altering the distribution of Foxp3+ regulatory T cells results in tissue-specific inflammatory disease

Blythe D. Sather1,2, Piper Treuting3, Nikole Perdue1, Mike Miazgowicz2, Jason D. Fontenot2, Alexander Y. Rudensky2, and Daniel J. Campbell1,2

1 Benaroya Research Institute, Seattle, WA 98101
2 Department of Immunology and 3 Department of Comparative Medicine, University of Washington School of Medicine, Seattle, WA 98195

CORRESPONDENCE Daniel J. Campbell: campbell{at}benaroyaresearch.org

CD4+Foxp3+ regulatory T cells (T reg) are essential for maintaining self-tolerance, but their functional mechanisms and sites of action in vivo are poorly defined. We examined the homing receptor expression and tissue distribution of T reg cells in the steady state and determined whether altering their distribution by removal of a single chemokine receptor impairs their ability to maintain tissue-specific peripheral tolerance. We found that T reg cells are distributed throughout all nonlymphoid tissues tested, and are particularly prevalent in the skin, where they express a unique CCR4+CD103hi phenotype. T reg cell expression of CCR4 and CD103 is induced by antigen-driven activation within subcutaneous lymph nodes, and accumulation of T reg cells in the skin and lung airways is impaired in the absence of CCR4 expression. Mice with a complete loss of CCR4 in the T reg cell compartment develop lymphocytic infiltration and severe inflammatory disease in the skin and lungs, accompanied by peripheral lymphadenopathy and increased differentiation of skin-tropic CD4+Foxp3+ T cells. Thus, selectively altering T reg cell distribution in vivo leads to the development of tissue-specific inflammatory disease.

Abbreviations used: APC, antigen-presenting cell; CT, cholera toxin; LC, Langerhans cell; PLN, peripheral LN; MLN, mesenteric LN.


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