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J Exp Med. 2002 Apr 1;195(7):855-67.

Resident skin-specific gammadelta T cells provide local, nonredundant regulation of cutaneous inflammation.

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Department of Dermatology and the Yale Skin Diseases Research Core Center, Yale University, New Haven, CT 06520, USA.


The function of the intraepithelial lymphocyte (IEL) network of T cell receptor (TCR) gammadelta(+) (Vgamma5(+)) dendritic epidermal T cells (DETC) was evaluated by examining several mouse strains genetically deficient in gammadelta T cells (delta(-/-) mice), and in delta(-/-) mice reconstituted with DETC or with different gammadelta cell subpopulations. and mice spontaneously developed localized, chronic dermatitis, whereas interestingly, the commonly used C57BL/ strain did not. Genetic analyses indicated a single autosomal recessive gene controlled the dermatitis susceptibility of mice. Furthermore, allergic and irritant contact dermatitis reactions were exaggerated in, but not in C57BL/ mice. Neither spontaneous nor augmented irritant dermatitis was observed in FVB.beta(-/-) delta(-/-) mice lacking all T cells, indicating that alphabeta T cell-mediated inflammation is the target for gammadelta-mediated down-regulation. Reconstitution studies demonstrated that both spontaneous and augmented irritant dermatitis in mice were down-regulated by Vgamma5(+) DETC, but not by epidermal T cells expressing other gammadelta TCRs. This study demonstrates that functional impairment at an epithelial interface can be specifically attributed to absence of the local TCR-gammadelta(+) IEL subset and suggests that systemic inflammatory reactions may more generally be subject to substantial regulation by local IELs.

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