Treatment update for vitiligo based on autoimmune inhibition and melanocyte protection

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.

This review discusses the latest knowledge on the pathogenesis of vitiligo and potential therapeutic targets from the perspective of suppressing autoimmune attacks and activating melanocytes functions.

Vitiligo is one of the most challenging dermatological diseases due to its complex pathogenesis with diverse therapeutic targets. Immune suppression, such as corticosteroids and emerging JAK inhibitors, has proven effective in disease progression. However, during the early stages of the disease, it is also important to optimize therapeutic strategies to activate melanocytes for alleviating oxidative stress and improving treatment outcomes.