Vitiligo is a chronic autoimmune depigmentation disorder affecting up to 152 million people worldwide, with increased prevalence among skin of color individuals in whom the disease is more noticeable. It has a profound negative impact on patient quality of life and lacks effective therapeutic options. While the current pathogenic paradigm highlights T H 1/IFNgupregulation, limited blood data also suggests possible involvement of other cytokine axes. We sought to investigate the genomic profile in lesional and non-lesional tissues of patients with vitiligo (n¼16) as compared with control skin (n¼8). We found significant upregulation of multiple immune pathways in both lesional and non-lesional vitiligo skin versus controls. These included significant increases in T H 1 markers (i.e. IFNg, CXCL9, CXCL10, and CCL5; p<0.01), but also in key T H 2 cytokines and chemokines (i.e. IL-5, IL-13; p<0.05, CCL13, and CCL18; p<0.01). Less consistent and significant increases were detected in some T H 17/T H 22 markers (i.e. IL-17A, IL-22, and S100A9; p<0.05), mostly in lesional skin only. Key mediators of JAK/STAT signaling (JAK3, STAT1) were significantly upregulated in both lesional and nonlesional tissues, as was the general inflammation marker MMP12 (p<0.05 for all). Overall, our data expands the current understanding of cytokine pathways in vitiligo skin beyond T H 1 skewing, providing a basis for possible future therapeutic targeting for patients with vitiligo.
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