Abstract

Vitiligo is an acquired and polygenetic autoimmune disorder with limited effective treatments. Dermal fibroblasts play a key role in vitiligo by responding to interferon-γ (IFN-γ) and secreting chemokines to recruit and activate CD8 + T cells. Although narrowband ultraviolet B (NB-UVB) is a common treatment for vitiligo, it can cause side effects such as phototoxicity. This study investigated the relationship between NB-UVB and fibroblast senescence in vitiligo and the mechanisms by which NB-UVB may trigger disease progression in some cases of vitiligo. Analysis of publicly available single-cell and bulk RNA sequencing data revealed that NB-UVB irradiation induces dermal fibroblast senescence and activates both the MAPK and p53 pathways. In vitro , high-dose NB-UVB exposure leads to increased senescence and inflammation in vitiligo fibroblasts. In vitiligo mice, low-dose NB-UVB treatment significantly reduced the number of CD8 + T cells and increased skin pigmentation. In contrast, high-dose NB-UVB induces a senescent, proinflammatory microenvironment and exacerbates vitiligo progression in some cases. In mouse skin, high-dose NB-UVB treatment induces cell senescence, and the expression of chemokines and cytokines increases, thereby disrupting the skin microenvironment and homeostasis.