Network of Dermatology Research (NDR), Universal Scientific Education and Research Network (USERN), Tehran, Iran.
Center for Research & Training in Skin Diseases & Leprosy, Tehran University of Medical Sciences, Tehran, Iran.
Adv Exp Med Biol. 2022;1367:19-59. doi: 10.1007/978-3-030-92616-8_2.
Alopecia areata (AA) is an autoimmune disease that targets the hair follicles (HF) and results in non-scarring hair loss. AA results from the collapse of the HF's immune privilege due to a combination of environmental and genetic factors that either change the local HF dynamics or dysregulate the central immune tolerance. Multiple genetic studies have attempted to identify AA susceptibility genes through candidate gene approaches and genome-wide analysis. These studies were able to show an association between AA and multiple immune-related genes such as those encoding cytokines, chemokines, molecules involved in regulatory T-cell functions, and adaptor molecules along with genes involved in autophagy, melanogenesis, and hair cycling pathways. This chapter aims to explore these genes and their contribution to the pathogenesis of the AA.
斑秃(AA)是一种自身免疫性疾病,其靶器官为毛囊(HF),导致非瘢痕性脱发。AA 是由于环境和遗传因素的共同作用,导致 HF 的免疫豁免崩溃,这些因素改变了局部 HF 的动态或调节了中枢免疫耐受。多项遗传研究试图通过候选基因方法和全基因组分析来鉴定 AA 的易感基因。这些研究表明,AA 与多种免疫相关基因之间存在关联,如细胞因子、趋化因子、参与调节性 T 细胞功能的分子以及衔接分子,以及参与自噬、黑色素生成和毛发周期途径的基因。本章旨在探讨这些基因及其在 AA 发病机制中的作用。