PD-L1 reverses depigmentation in Pmel-1 vitiligo mice by increasing the abundance of Tregs in the skin

• Published in: Scientific reports 2018-01, Vol.8 (1), p.1605-6, Article 1605
• Main Authors: Miao, Xiao, Xu, Rong, Fan, Bin, Chen, Jie, Li, Xin, Mao, Weiwei, Hua, Shengyuan, Li, Bin
• Format: Article
• Language: English
• Subjects: 13; 13/1; 13/31; 14; 14/34; 14/63; 38; 38/1; 631/250/38; 631/80/86; Animals; Apoptosis; B7-H1 Antigen - administration & dosage; Cell death; Fusion protein; Humanities and Social Sciences; Immune checkpoint; Immune response; Immunoregulation; L1 protein; Ligands; Lymphocytes T; Mice; multidisciplinary; PD-1 protein; PD-L1 protein; Proteins; Recombinant Fusion Proteins - administration & dosage; Science; Science (multidisciplinary); Skin; Skin - pathology; Skin diseases; Spleen; T-Lymphocytes, Regulatory - immunology; Treatment Outcome; Vitiligo; Vitiligo - pathology; Vitiligo - therapy
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-018-19407-w

Programmed cell death 1 ligand 1 (PD-L1) is a ligand of programmed cell death 1 (PD-1) that functions as an immune checkpoint by down-regulating immune responses. To determine whether PD-L1 is a therapy target in vitiligo treatment, Pmel-1 vitiligo mice were treated with a PD-L1 fusion protein. Treatment with this fusion protein significantly reversed/suppressed depigmentation development in adult Pmel-1 mice. Mechanistically, enrichment of regulatory T cells (Treg) in the skin was detected after PD-L1 fusion protein treatment in Pmel-1 mice. Furthermore, Tregs abundance was also increased in both the spleen and circulation of Pmel-1 mice treated with PD-L1. These data indicate that PD-L1 protein therapy inhibits the immune response and reverses depigmentation development in Pmel-1 vitiligo mice.