Dichotomy of blood- and skin-derived IL-4-producing allergen-specific T cells and restricted V beta repertoire in nickel-mediated contact dermatitis.

In this study we compared the phenotype and cytokine patterns of nickel-specific T cell clones (TCC) derived from blood samples and positive patch test reactions. A total of 252 nickel-specific TCC were established from three nonatopic patients with allergic contact dermatitis caused by nickel. All TCC expressed the TCR-alpha beta, and 77% were CD4+ compared with 21% CD8+ TCC. In contrast to blood-derived TCC, the majority of skin-derived CD4+ or CD8+ T lymphocytes produced IL-4 either in combination with IFN-gamma (type 0 cytokine pattern) or IL-4 exclusively (type 2 pattern). Skin-derived nickel-specific TCC of each patient secreted significantly more IL-4 than blood-derived TCC of the same individual. Analysis of TCR-V beta repertoire from two patients indicated that >40% of the tested TCC expressed one of the following V beta elements: V beta 13.1/13.2, V beta 20, V beta 2, V beta 6.7, or V beta 14. Only 20% of unstimulated T cells but >40% of nickel-stimulated T cells derived from peripheral blood of the same individuals expressed these V beta elements, suggesting a selection of certain TCR-V beta elements by nickel sulfate in these patients. In contrast to the compartmentalization of IL-4 production, there were no major differences in the expression of TCR-V beta elements between blood- and skin-derived nickel-specific TCC. These results point to a modulation of the cytokine production pattern of T lymphocytes after their migration from peripheral blood into the skin and a production of the type 2 cytokine IL-4 in acute eczematous lesions in nonatopic individuals.