黑素细胞破坏或凋亡导致白癜风发病的机制是皮肤科研究热点之一。前期课题组研究证实：H2O2诱导氧化应激时，黑素细胞中的钙网织蛋白（CRT）翻转至细胞膜表面，诱导免疫原性增强，促进炎症因子表达，激活后续免疫应答，进一步对黑素细胞产生攻击。CRT又称cC1qR，是补体C1q的主要受体之一，C1q另一受体gC1qR可调控细胞凋亡，而CRT/gC1qR复合体在持续氧化应激诱导细胞损伤中的作用尚不明确。为探讨CRT/gC1qR复合体在氧化应激诱导白癜风发病中的机制，拟构建白癜风三维表皮模型及白癜风小鼠模型，深入研究CRT、gC1qR在角质形成细胞和黑素细胞中的表达模式及重要功能，明确CRT、gC1qR、CRT/gC1qR复合体在表皮细胞应对氧化损伤中的重要作用，有助于阐明氧化应与异常免疫应答的"桥梁"机制，为研究白癜风发病机制、指导疾病防治提供重要依据。

The mechanism of melanocyte destruction or apoptosis in vitiligo is one of the current research focuses in dermatology. The ongoing project supposes that oxidative stress may be the primary factor in the pathogenesis of vitiligo vulgaris. Oxidative stress induces melanocyte damage and immunogenic enhanced, which promote autoimmune responses. Preliminary experiments suggested that CRT in melanocytes translocated on the melanocytes membrane after H2O2 induced oxidative stress. The translocation of CRT further stimulates melanocyte damage attacked by immunity. CRT, also known cC1qR, is one of the main receptor of complement C1q, and the another receptor gC1qR have an important role in apoptosis. Role of CRT/gC1qR complex in oxidative stress-induced cell damage is still controversial. To explore CRT/gC1qR complex function in oxidative stress mediated melanocyte damage, we plans to construct a vitiligo three-dimensional epidermal model and vitiligo mouse, and study the CRT, gC1qR expression patterns in keratinocytes and melanocytes, thus elucidate the role of the CRT, gC1qR and CRT/gC1qR complex in oxidative stress induced cell damage. The results help to clarify the mechanism of oxidative stress and abnormal immune response in vitiligo, and provide important basis for vitiligo prevention and treatment.