Breaking tolerance to nickel.

Abstract

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.