Ruolo dello zinco nella modulazione della risposta immune nella dermatite da contatto da nichel

Nickel is the most common allergen in contact dermatitis. It is a transition metal that is related by nickel-containing alloys and absorbed intercellularly. This has been well documented in vitro, using mouse and human lymphocytes. The onset of nickel contact dermatitis varies according to the type of nickel salt, nickel oxidation states (Ni II and Ni III interacts mainly with biological systems), and the configuration. Recently, it has been reported that topical and oral administration of zinc sulphate reduces or eliminates clinical manifestations of nickel dermatitis and nickel patch test reactions in nickel-positive subjects. The mechanism of zinc immunomodulation is still uncleared: in nickel dermatitis, zinc sulphate may compete in peptide and protein interaction, preventing the antigen production or might act on its anti-oxidant and anti-inflammatory properties. In this study, the zinc-nickel interaction was evaluated, estimating the ability of zinc sulphate to interfere in vitro, with the lymphomonocytic cytokine production (INF-γ, IL-1β, IL-10). The results showed that nickel induced a TCD4+ cell proliferation as well as INF-γ and IL-1β release by lymphomonocytes in allergic and healthy subjects. Zinc sulphate inhibited this release and stimulated IL-10 production (an immunomodulation cytokine) by lymphomonocytes. In conclusion, it is possible that the immunomodulant and anti-inflammatory effect from zinc salt is due to its influence on cytokine production, especially on IL-10 release.