Abstract
Vitiligo is an inflammatory disease that presents as well-demarcated, depigmented skin lesions. While different mechanisms are implicated in the development and maintenance of vitiligo lesions, immune-mediated destruction of melanocytes has been ascribed the major mechanism of depigmentation. We have previously observed enrichment of cytotoxic resident CD49a+ CD103+ T-cells in the skin of vitiligo patients and recent single cell data highlights crosstalk between CD8+ effector and Treg cells within the lesion, as well as a subclinical state of activation in the non-lesional skin.
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