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The Journal of Immunology, 2001, 167: 6038-6044.
Copyright © 2001 by The American Association of Immunologists

Preferential Usage of TCR-V{beta}17 by Peripheral and Cutaneous T Cells in Nickel-Induced Contact Dermatitis1

Lioba Büdinger*,{dagger}, Nicole Neuser*, Uwe Totzke{ddagger}, Hans F. Merk* and Michael Hertl2,*,§

* Department of Dermatology and {dagger} Interdisciplinary Center for Clinical Research, Rheinisch-Westfälische Technische Hochschule, Aachen, Germany; {ddagger} MDS Pharma Services, Hamburg, Germany; and § Department of Dermatology, University ofErlangen, Erlangen, Germany

Nickel (Ni) is one of the most common contact sensitizers in man, and Ni-induced contact dermatitis is considered as a model of hapten-induced delayed type hypersensitivity. Previous studies indicated that Ni-reactive T cells derived from Ni-allergic individuals preferentially express distinct TCR-V{beta} chains. However, data on the TCR-V{beta} repertoire of Ni-responsive T cells are not consistent. Therefore, the aim of this study was to identify the TCR-V{beta} receptors of Ni-responsive peripheral and cutaneous T cells in a cohort of 17 donors with Ni-induced contact dermatitis in comparison with those of 6 healthy controls. Peripheral NiSO4-responsive T lymphocytes showed a significant overexpression of TCR-V{beta}17 and the frequency of TCR-V{beta}17+ T cells correlated significantly with the in vitro reactivity of PBMC to NiSO4. In addition, the cutaneous infiltrate of Ni-induced patch test reactions consisted primarily of V{beta}17+ T cells. The majority of patch test-derived NiSO4-responsive T cells of three allergic donors were TCR-V{beta}17+, whereas patch test-derived NiSO4 unresponsive T cells of four additional donors did not express TCR-V{beta}17. Skin-derived Ni-responsive T cell lines from three donors uniformly secreted the Th2 cytokine, IL-5, but no IFN-{gamma} or IL-10. These in vitro and in vivo findings strongly suggest that T cells with a restricted TCR-V{beta} repertoire, i.e., V{beta}17, predominate in NiSO4-induced contact dermatitis and may be crucial in the effector phase of Ni hypersensitivity.




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