Tissue Preservation, Life care and Biobanking (B2B & Networking)

Vitiligo is an autoimmune depigmentation disorder characterized by white spots on the skin that cause profound social and psychologic stigma in patients. Vitiligo is caused by CD8+ T cell-mediated destruction of epidermal melanocytes (MCs). Vitiligo repigmentation requires proliferation and migration of MC precursors from the hair follicle (HF) bulge to repopulate the interfollicular epidermis, and the strongest stimulus for this process is Narrow Band UVB (NBUVB). To better understand this process, we developed a research platform that used skin biopsies collected from 6 vitiligo patients treated with NBUVB and 6 untreated vitiligo patients, using rapid fluorescent immunostaining combined with laser capture microdissection to collect RNA from bulge MC precursors and mature MCs from the epidermis of the regenerated vitiligo skin. The total RNA captured from MCs was subjected to whole transcriptome RNA sequencing, followed by gene expression analysis. We found upregulation of TNC, GJB6 and THBS1 transcripts in the bulge MC precursors of NBUVB-treated vitiligo skin as compared with epidermal MCs of regenerated NBUVB-treated vitiligo skin, and of β-catenin as being the top upstream transcription regulator of this process. We also identified that GLI1, a candidate stem cell-associated gene, was significantly modulated by NBUVB in the bulge MCs. The above pathway and signals are potentially key-players in the activation of bulge MC precursors during vitiligo repigmentation.