Many studies have shown the involvement of interferon (IFN)γ-inducible protein 10 (IP-10) and T-helper 1 (Th1) cytokines in Atopic Dermatitis (AD). IFN-γ, tumor necrosis factor (TNF)-α and interleukin (IL)-18 are potent stimulators of the expression and secretion of IP-10 in cultured keratinocytes from AD patients. Apoptosis of keratinocytes, induced mainly by T cells and mediated by IFN-γ, is the essential pathogenetic event in eczema formation. Enhanced IP-10, induced by IFN-γ, and IFN-inducible T cell alpha-chemoattractant (I-TAC) expression has been observed in lesional AD skin. It has been shown that keratinocytes undergoing apoptosis in acute eczematous lesions release chemokines that attract more T cells toward the epidermis, which may further augment the inflammation and keratinocyte apoptosis. Drugs used in the treatment of AD modulate IP-10. Antihistamines are widely used for the treatment of AD; it has been shown in human monocyte-derived dendritic cells (MoDCs) and autologous CD4+ T cells that antihistamines inhibited the production of IP-10 and�� monokine induced by IFN-gamma (MIG) expressions. It has been also shown that antimycotics and tacrolimus suppress the induced production of IP-10 in human keratinocytes.
Keywords: Atopic dermatitis; Chemokine; IFN-γ; IP-10; Th1.