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Long Siyu, Wang Hongsheng, Yu Meiwen Department of Leprosy Control, Hospital of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, National Center for Leprosy Control, Chinese Center for Diseases Control and Prevention, Nanjing 210042, China (Long SY, Yu MW); Laboratory of Leprosy and Other Mycobacterial Infections, Hospital of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, National Center for Leprosy Control, Chinese Center for Diseases Control and Prevention, Nanjing 210042, China��Wang HS�� Corresponding author: Yu Meiwen, Email: yumeiwen@163.com ��Abstract�� Vitiligo is a depigmented skin disease, characterized by the destruction of functional melanocytes in the epidermis. Present studies have proved that the occurrence of vitiligo is associated with genetics, immunity, oxidative stress, neural and humoral mechanisms and so on. Among these mechanisms, T cell?mediated immune responses play an important role in the occurrence of vitiligo. The CD4+ T cell subsets, including T?helper 1 ��Th1�� cells, Th2 cells, Th17 cells and regulatory T ��Treg�� cells, can regulate the function of other immune cells and induce apoptosis of melanocytes by secreting various cytokines. CD8+ T cells can directly kill melanocytes by exerting cytotoxic effects. On the other side, the breakdown of autotolerance, increased number and activity of autoreactive T cells can enhance the T cell immune response against melanocytes. Besides these mechanisms, invariant natural killer T cells and memory T cells both play a certain role in the immunological pathogenesis of vitiligo.