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

• DOI: 10.1084/jem.20070081
• Publication Date: 2007-06-05T00:55:17Z
• Authors: Blythe D. Sather; Piper Treuting; Nikole Perdue; Mike Miazgowicz; Jason D. Fontenot; Alexander Y. Rude...; Daniel J. Campbell
• Keywords: CCR4; Peripheral tolerance

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