Breaking tolerance to nickel.
Nickel is a ubiquitous metal frequently responsible of allergic skin reactions. Development of undesired reaction to nickel has been positively correlated with the expansion of specific CD8+ T cells, that induce apoptosis of nickel-loaded keratinocytes through a perforin-dependent mechanism. In non allergic individuals, the lack of circulating CD8+ T cells reactive to nickel, as well as the absence of inflammatory responses at the site of skin exposure to the metal are the consequence of the expansion of specialized T cells with regulatory function. Among these, CD4(+)CD25+ T cells from peripheral blood of non allergic subjects strongly regulate immune responses to nickel in a cytokine-independent, cell-contact-dependent mechanism. In contrast, CD4(+)CD25+ obtained from the blood of nickel-allergic individuals have limited or absent suppressive activity on specific T cell responses in vitro.
Cavani
Andrea
A
Laboratory of Immunology, IDI-IRCCS, Via Monti di Creta 104, 00167 Roma, Italy. cavani@idi.it
D000818:Animals; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D017449:Dermatitis, Allergic Contact / Q000276:immunology*; D006801:Humans; D009532:Nickel / Q000276:immunology / Q000633:toxicity*
D009532:Nickel