Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 142, Issue 4, Pages 1194-+Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jid.2021.09.015
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Funding
- Agence nationale de la recherche Young Researchers JCJC (ANR VIEMTEC)
- Sanofi
- Societe Francaise de Dermatologie grants
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Vitiligo is a complex skin disorder involving both immune responses and melanocyte dysfunction. In addition to being targeted by T cells, melanocytes may actively contribute to the inflammation process. Jak inhibitors have the potential to prevent the impact of T cells on skin cells and pigmentation, offering clinical benefits for vitiligo treatment.
Vitiligo is a T cellemediated inflammatory skin disorder characterized by the loss of epidermal melanocytes. However, the contribution of melanocytes to the physiopathology of the disease in response to the T-cell microenvironment remains unclear. Here, using NanoString technology and multiplex ELISA, we show that active vitiligo perilesional skin is characterized by prominent type 1 and 2 associated immune responses. The vitiligo skin T-cell secretome downregulated melanocyte function and adhesion while increasing melanocyte mitochondrial metabolism and expression of inflammatory cytokines and chemokines by epidermal cells. The Jak1/2 inhibitor ruxolitinib strongly inhibited such effects on epidermal cells. Our data highlight that vitiligo is more complex than previously thought, with prominent combined activities of both T helper type 1e and T helper type 2erelated cytokines inducing inflammatory responses of epidermal cells. Melanocytes do not appear only to be a target of T cells in vitiligo but could actively contribute to perpetuate inflammation. Jak inhibitors could prevent the impact of T cells on epidermal cells and pigmentation, highlighting their potential clinical benefit in vitiligo.
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