CXCR3型
白癜风
CXCL10型
CXCL9型
生物
趋化因子
免疫学
趋化因子受体
发病机制
调解人
细胞生物学
免疫系统
作者
Hanqing Liu,Yihui Wang,Qianqian Le,Jiajia Tong,Honglin Wang
标识
DOI:10.1002/eji.202250281
摘要
Abstract Vitiligo is a disease featuring distinct white patches that result from melanocyte destruction. The overall pathogenesis of vitiligo remains to be elucidated. Nevertheless, considerable research indicates that adaptive immune activation plays a key role in this process. Specifically, the interferon‐gamma (IFN‐γ), C‐X‐C motif chemokine ligands (CXCL9/10), and C‐X‐C motif chemokine receptor (CXCR3) signaling axis, collectively referred to as IFN‐γ‐CXCL9/10‐CXCR3 or ICC axis, has emerged as a key mediator responsible for the recruitment of autoimmune CXCR3 + CD8 + T cells. These cells serve as executioners of melanocytes by promoting their detachment and apoptosis. Moreover, IFN‐γ is generated by activated T cells to create a positive feedback loop, exacerbating the autoimmune response. This review not only delves into the mechanistic insights of the ICC axis but also explores the significant immunological effects of associated cytokines and their receptors. Additionally, the review provides a thorough comparison of existing and emerging treatment options that target the ICC axis for managing vitiligo. This review aims to foster further advancements in basic research within related fields and facilitate a deeper understanding of alternative treatment strategies targeting different elements of the axis.
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