The immunology of nickel-induced allergic contact dermatitis.

ABSTRACT

Attempts have been made to elucidate the immunopathogenesis of contact allergy; yet, the exact mechanism by which nickel-induced allergic contact dermatitis (NACD) occurs is far from clear and is discussed herein. It seems to suggest that a direct nickel-MHC class II molecule binding on the skin antigen presenting cells such as Langerhans cells (LCs) would result in Th1 cell activation. Substances such as serotonin and cytokines such as TNF-alpha produced by activated mast cells may increase adhesion molecule expression and thus, enhance T cell trafficking in the skin. Cytokines such as IFN-gamma and IL-1 and perhaps IL-12 certainly play a crucial role in the activation of Th1 cells. Along with possible function of CD8 cells, downregulation of NACD may be mediated by suppressed function of LCs via the action of activated keratinocytes-derived IL-10. Inhibition of NACD can also be generated by feeding with nickel, suggesting that the induction of oral tolerance to nickel may be beneficial for an alternative immunotherapy of nickel allergy. Nevertheless, this testable model provides a direction for further investigation.