Contact dermatitis and interferon-γ dependent chemokines.

Abstract

Inflammation of the skin is the pathological base of contact dermatitis (CD), and cytokines are very important in its pathogenesis. Recently it has been shown that interferon (IFN)-γ, and the IFN-γ dependent chemokines, monokine induced by IFN-γ (MIG), IFN-γ-induced protein 10 (IP-10), and IFN-inducible T cell alpha chemoattractant (I-TAC), play an important role in CD. Allergic CD (ACD) is a T-cell-mediated disease in which expression of a distinct repertoire of chemokines results in the recruitment of effector T cells into the skin. An increased expression of MIG, IP-10 and I-TAC in the skin has been observed by many studies in ACD, but not in irritant CD. The IFN-γ dependent chemokines are produced by keratinocytes, mainly during the clinically inflammatory phase of ACD. Also chemokine (C-X-C motif) receptor (CXCR) 3, the common receptor of the three IFN-γ dependent chemokines, is upregulated in chemical-induced allergic skin responses when compared with irritant skin responses. However, other studies have shown a low level increase of IP-10 in irritant sodium dodecyl sulphate dermatitis. The above mentioned results show that although skin inflammation contact sensitizer-induced is similar to irritant-induced, the regulation of allergic inflammation-related gene MIG and IP-10, could help to discriminate skin sensitization from chemically irritation.