Lymphoid Stress Surveillance Response Contributes to Vitiligo Pathogenesis

摘要: Vitiligo is a chronic multifactorial depigmentation disorder characterized by the destruction and functional loss of melanocytes. Although direct cytotoxic T cell attack thought to be responsible for melanocyte damage, events leading self-tolerance toward melanocytic antigens are not understood. This research aimed identify novel cellular molecular factors that participate in vitiligo pathogenesis through application gene expression immunofluorescence analysis skin biopsy samples along with immunophenotyping circulating cells. Our study provides insights into mechanisms involved destruction. The upregulation stress-ligand MICA/MICB, recognized activating receptors on innate innate-like cells, imply involvement lymphoid stress surveillance responses lesions. A simultaneous increase transcription factor EOMES characteristic virtual memory suggest similar scenario. Local has been previously associated amplification systemic humoral were mirrored our increased follicular helper cells switched B proportions patients active vitiligo. In addition, microtubule-associated protein light chain 3 staining was compatible activation autophagy keratinocytes remaining melanocytes lesional skin.