Preferential usage of TCR-V beta 17 by peripheral and cutaneous T cells innickel-induced contact dermatitis

Citation
L. Budinger et al., Preferential usage of TCR-V beta 17 by peripheral and cutaneous T cells innickel-induced contact dermatitis, J IMMUNOL, 167(10), 2001, pp. 6038-6044
Citations number
30
Categorie Soggetti
Immunology
Journal title
JOURNAL OF IMMUNOLOGY
ISSN journal
00221767 → ACNP
Volume
167
Issue
10
Year of publication
2001
Pages
6038 - 6044
Database
ISI
SICI code
0022-1767(20011115)167:10<6038:PUOTB1>2.0.ZU;2-K
Abstract
Nickel (Ni) is one of the most common contact sensitizers in man, and Ni-in duced 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 reactiv ity of PBMC to NiSO4. In addition, the cutaneous infiltrate of Ni-induced p atch test reactions consisted primarily of V beta 17(+) T cells. The majori ty 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-r esponsive T cell lines from three donors uniformly secreted the Th2 cytokin e, IL-5, but no IFN-gamma or IL-10. These in vitro and in vivo findings str ongly 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 crucia l in the effector phase of Ni hypersensitivity.