Investigating the effect of phototherapy on gene expression of CXCR3-B in Vitiligo

Abstract

Summary Vitiligo is acquired depigmentary disorder characterized by destruction of the epidermal melanocytes leading to the loss of the skin color. Oxiditive stress, genetic susceptibility together with autoimmunity are the main players of aetiopathogenesis and melanocytic destruction. Innate immunity triggers early immune responses against melanocytes in non-segmental vitiligo as It is well demonstrated that vitiligo melanocytes possess higher susceptibility to oxidative insults that trigger IFNγ production from Natural killer ‘NK ‘and innate lymphoid cells. Melanocytes of vitiligo patients show an increased basal expression of CXCR3B receptor compared to normal melanocytes and respond to INF γ upregulating their chemokine production of CXCL10, CXCL9, CXCL11 and subsequent recruitment of CD8+ T cells expressing CXCR3. CXCR3 is a chemokine receptor expressed on autoreactive T cells and is upregulated upon activation with antigen and recruits activated cells to sites of tissue inflammation in response to its primary CXCL10 leading to the accumulation of CXCR3+T cells with Th1 phenotypes. In inflamed tissues recruited Th1 lymphocytes are responsible for enhanced IFN-γ, which in turn stimulate further CXCL10 secretion from a variety of cells including neutrophils and lymphocytes therefore creating an amplification feedback loop responsible for the loss of melanocytes.