Breaking tolerance to nickel

Andrea Cavani

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)119-121
Number of pages3
Issue number2
Publication statusPublished - Apr 15 2005


  • Allergic contact dermatitis
  • Nickel
  • Regulatory T cells

ASJC Scopus subject areas

  • Toxicology


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