DICHOTOMY OF BLOOD-DERIVED AND SKIN-DERIVED IL-4-PRODUCING ALLERGEN-SPECIFIC T-CELLS AND RESTRICTED V-BETA REPERTOIRE IN NICKEL-MEDIATED CONTACT-DERMATITIS
T. Werfel et al., DICHOTOMY OF BLOOD-DERIVED AND SKIN-DERIVED IL-4-PRODUCING ALLERGEN-SPECIFIC T-CELLS AND RESTRICTED V-BETA REPERTOIRE IN NICKEL-MEDIATED CONTACT-DERMATITIS, The Journal of immunology, 158(5), 1997, pp. 2500-2505
In this study we compared the phenotype and cytokine patterns of nicke
l-specific T cell clones (TCC) derived from blood samples and positive
patch test reactions, A total of 252 nickel-specific TCC were establi
shed from three nonatopic patients with allergic contact dermatitis ca
used by nickel, All TCC expressed the TCR-alpha beta, and 77% were CD4
(+) compared with 21% CD8(+) TCC, In contrast to blood-derived TCC, th
e 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 e
ach patient secreted significantly more IL-4 than blood-derived TCC of
the same individual, Analysis of TCR-V beta repertoire from two patie
nts indicated that >40% of the tested TCC expressed one of the followi
ng 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-sti
mulated 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 t
he compartmentalization of IL-4 production, there were no major differ
ences in the expression of TCR-V beta elements between blood- and skin
-derived nickel-specific TCC, These results point to a modulation of t
he cytokine production pattern of T lymphocytes after their migration
from peripheral blood into the skin and a production of the type 2 cyt
okine IL-4 in acute eczematous lesions in nonatopic individuals.