Treatment update for vitiligo based on autoimmune inhibition and melanocyte protection

Introduction The treatment of vitiligo remains challenging due to the complexity of its pathogenesis, influenced by genetic factors, oxidative stress and abnormal cell adhesion that collectively impact melanocyte survival and trigger immune system attacks, resulting in melanocyte death. Melanocytes in vitiligo are believed to exhibit genetic susceptibility and defects in cellular mechanisms, such as defects in autophagy, that reduce their ability to resist oxidative stress, leading to increased expression of the pro-inflammatory protein HSP70. The low expression of adhesion molecules, such as DDR1 and E-cadherin, accelerates melanocyte damage and antigen exposure. Consequently, autoimmune attacks centered on IFN-γ-CXCR9/10-CXCR3-CD8+ T cells are initiated, causing vitiligo.