白癜风是一种自身免疫性皮肤病，情绪应激可导致其快速发展，但机制不清。研究证实，神经肽Galanin在皮肤局部识别其受体，可引起异常免疫应答。我们发现：白癜风患者皮肤局部神经肽Galanin及其受体表达均显著升高，初步证实Galanin可促进黑素细胞膜表面自身抗原蛋白表达，并促进患者外周血CD8+T细胞活化，参与白癜风黑素细胞免疫损伤。基于前期研究及文献，我们提出科学假说：白癜风皮肤中Galanin高表达，通过其受体与黑素细胞及CD8+T细胞cross talk，促进CD8+T细胞对黑素细胞特异性杀伤，导致白癜风发生发展。本项目拟扩大样本明确白癜风患者Galanin及其受体的表达，进一步结合临床样本、体外细胞及白癜风小鼠模型，利用定量蛋白质组学、免疫荧光等技术手段，阐明其在介导白癜风免疫应答中的作用及分子机制，对系统阐明白癜风的发生发展机制、寻找新的白癜风靶向干预治疗措施具有重要意义。

Vitiligo is an autoimmune skin disease, and emotional stress can lead to its rapid development, however, the specific mechanism has not been elucidated. Previous studies indicated that the neuropeptide Galanin recognized specific receptors in the skin and caused skin inflammatory response. We found that the expression and secretion of Galanin and its receptor were both significantly up-regulated in vitiligo patients. Besides, Galanin stimulation significantly promoted the expression of autoantigen protein on the membrane surface of melanocyte (MC) and CD8+ T cell activation. Based on previous studies and literature, we hypothesize that the expression of Galanin in vitiligo skin is increased, and it could promote MC antigen exposure and CD8+ T cell activation by its receptor-mediated key molecules, ultimately leading to MC-specific killing and promote the occurrence and development of vitiligo. To verify this hypothesis, we plan to expand the sample to determine the expression of Galanin and its receptors in patients with vitiligo. Moreover, we will further combine clinical samples, in vitro cells and vitiligo mouse models, using quantitative proteomics, immunofluorescence and other techniques to elucidate its role and molecular mechanism in mediating vitiligo immune response. The project is of great significance for comprehensively elucidating the mechanism of occurrence and development of vitiligo and searching for new vitiligo targeted treatment.