Abstract
Vitiligo is an acquired immune disorder of the skin characterized by the presence of white depigmented macules. Its immunopathogenesis is not completely understood, but inflammatory alterations in the skin microenvironment, and particularly increased expression of the cytokine tumor necrosis factor-α (TNFα), are thought to be essential regulators of melanocyte dysfunction and death. In this article we review the evidence that implicates TNFα in the pathogenesis of vitiligo, including studies on serum and tissue levels of TNFα, TNFα gene polymorphisms, in vitro studies, and therapeutic trials using TNFα inhibitors. TNFα emerges as a complex mediator with apparently conflicting roles in vitiligo.
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