Abstract：
Alopecia areata (AA) is characterized by common non-scarring alopecia due to autoimmune disorders. To date, the specific pathogenesis underlying AA remains unknown. Thus, AA treatment in the dermatological clinic is still a challenge. Numerous clinical observations and experimental studies have established that melanocytes may be the trigger point that causes hair follicles to be attacked by the immune system. A possible mechanism is that the impaired melanocytes, under oxidative stress, cannot be repaired in time and causes apoptosis. Melanocyte-associated autoantigens are released and presented, inducing CD8+ T cell attacks. Thereafter, amplification of the immune responses further spreads to the entire hair follicle (HF). The immune privilege of HF subsequently collapses, leading to AA. Herein, we present a narrative review on the roles of melanocytes in AA pathogenesis, aiming to provide a better understanding of this disease from the melanocyte\'s perspective.
摘要：
斑秃（AA）的特征是由于自身免疫性疾病引起的常见非瘢痕性脱发。迄今为止,AA的具体发病机制尚不清楚.因此，皮肤科诊所的AA治疗仍然是一个挑战。许多临床观察和实验研究已经确定，黑素细胞可能是导致毛囊受到免疫系统攻击的触发点。一个可能的机制是受损的黑素细胞，在氧化应激下，不能及时修复并引起细胞凋亡。黑素细胞相关的自身抗原被释放和呈递，诱导CD8+T细胞攻击。此后,免疫应答的扩增进一步扩散到整个毛囊(HF)。HF的免疫特权随后崩溃，导致AA。在这里，我们对黑素细胞在AA发病机制中的作用进行了叙述性综述，旨在从黑素细胞的角度更好地了解这种疾病。
