TH2-type infiltrating T cells in nickel-induced contact dermatitis.
The T cell response to nickel-modified endogenous peptides is involved in the immunopathogenesis of nickel-induced contact dermatitis. Nickel-reactive T cells described so far display a TH1 lymphokine secretion pattern characterized by high amounts of IFN gamma, but little or no IL-4 and IL-5. In this paper we demonstrate that nickel-reactive T cells can belong to the TH0 and even to the TH2 CD4+ T cell subset. Nickel-reactive T cell clones (TCC) were derived from the lesion of a patient with nickel contact dermatitis. These TCC responded to nickel with the production of high levels of IL-5 and variable amounts of IFN-gamma and IL-4 resembling TH2- or TH0-like cytokine secretion pattern. None of the nickel-reactive TCC showed a clear cut TH1 profile. We show that IL-4 was a growth factor for the TH2 and some of the TH0 TCC. We conclude that nickel is able to induce TH2 cells and that in this patient with a typical nickel-induced contact dermatitis TH2 cells are prevalent and might contribute to the immunopathogenesis of contact dermatitis.
Probst
P
P
Department of Medical Microbiology and Immunology, Bernhard-Nocht Institute for Tropical Medicine, Hamburg, Germany.
Küntzlin
D
D
Fleischer
B
B
D002461:Cell Line, Transformed; D002999:Clone Cells; D016207:Cytokines / Q000096:biosynthesis*; D017449:Dermatitis, Allergic Contact / Q000209:etiology* / Q000276:immunology; D003877:Dermatitis, Contact / Q000276:immunology*; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D015848:Interleukin-5 / Q000096:biosynthesis; D008213:Lymphocyte Activation / Q000276:immunology; D009532:Nickel / Q000009:adverse effects*; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D018418:Th2 Cells / Q000276:immunology* / Q000378:metabolism*
D016207:Cytokines; D015848:Interleukin-5; D015847:Interleukin-4; D009532:Nickel; D007371:Interferon-gamma