Membranal Expression of Calreticulin Induced by Unfolded Protein Response in Melanocytes: A Mechanism Underlying Oxidative Stress–Induced Autoimmunity in Vitiligo

• DOI: 10.1016/j.jid.2024.01.007
• Publication Date: 2024-01-21T00:36:55Z
• Authors: Pu Song; Weigang Zhang; Sen Guo; Gang Wang; Tianwen Gao; Chunying Li; Ling Liu
• Keywords: Vitiligo

Calreticulin (CRT), a damage-associated molecular pattern molecule, is reported to translocate from endoplasmic reticulum membrane in melanocytes under oxidative stress. To investigate the potential role of CRT pathogenesis vitiligo, we analyzed correlation between and ROS serum lesions detected protein kinase RNA-like ER (PERK) expression vitiligo lesions, studied production mediators unfolded response (UPR) pathway, then tested chemotactic migration CD8+ T cells or CD11c+ CD86+ cells. Initially, verified overexpression perilesional epidermis that was positively correlated with disease severity vitiligo. Furthermore, PERK branch UPR confirmed be responsible for membranal translocation We also found stress-induced promoted activation Additionally, dendritic patients were prone maturation co-incubation harboring CRT. could induced on via might play stress-triggered cell