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.
Original language | English |
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Pages (from-to) | 119-121 |
Number of pages | 3 |
Journal | Toxicology |
Volume | 209 |
Issue number | 2 |
DOIs | |
Publication status | Published - Apr 15 2005 |
Keywords
- Allergic contact dermatitis
- Nickel
- Regulatory T cells
ASJC Scopus subject areas
- Toxicology