الفهرس 
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Abstract
Vitiligo is an acquired, multifactorial, depigmenting disorder of the skin and mucous membranes characterized clinically by the appearance of circumscribed white depigmented macules and patches due to selective progressive destruction of functional melanocytes in the epidermis. It has a prevalence of approximately 0.5% to 1% of the population. The vitiligo may appear at any age, any race, and both men and women are both equally affected (Kyriakis et al., 2009).
It still unknown what causes damage and disappearance to melanocytes in affected skin. Depending on many theories, the cause of this is an overlap between many different factors, including, autoimmune, neurohumoral, autocytotoxic and genetic. These different factors can act independently or together to cause the disease (Laddha et al., 2013).
IL-36α belongs to IL-36-cytokine family, which is related to the IL-1-superfamily, it is proved that interleukin-36 have the same signals as IL-1 that have a role in organizing innate as well as adaptive immune responses. IL-36 agonists have a moderate maturing effect on DCs, induce IL-6, IL-12, IL-23 and it induces T cell polarization and plays a significant role in differentiation of Th0 cells into IFNγ-producing Th1 cells and Th17 responses, that involved in pathogenesis of vitiligo, thus suggesting the potential involvement of IL-36 in the development of vitiligo priming of immune responses in vitiligo patient (Vigne et al., 2012, Matti et al., 2013).