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Pharmacological solutions for vitiligo: emerging role of Janus kinase inhibitors.

Created on 08 Sep 2026

Authors

Hristina Kocic, Uwe Wollina, Aleksandar Godic, Vesna Karanikolic, Jelena Stojkovic-Filipovic, Masa Golubovic, Yan Valle, Torello Lotti

Published in

Expert opinion on pharmacotherapy. Sep 07, 2026. Epub Sep 07, 2026.

Abstract

Vitiligo is a chronic autoimmune condition characterized by progressive loss of melanocytes and the development of depigmented skin lesions. Increasing evidence highlights the pivotal role of dysregulated JAK-STAT signaling in disease pathogenesis.
A literature search was performed using PubMed/MEDLINE, to identify relevant studies published up to January 2026, about the contribution of JAK-STAT-dependent pathways to vitiligo progression, IFN-γ-induced chemokine production (CXCL9 and CXCL10), recruitment of cytotoxic CD8+ T lymphocytes, and the involvement of tissue-resident memory (T < sub>RM) T cells in maintaining localized immune responses. The effects of JAK inhibition across multiple cell populations, including melanocytes, keratinocytes, and immune cells were examined. Current clinical data regarding both topical and systemic JAK inhibitors in the context of targeted repigmentation strategies.
Unlike conventional systemic immunosuppressive therapies, JAK inhibitors enable targeted modulation of specific inflammatory pathways central to vitiligo pathophysiology. Future therapeutic success will likely depend on appropriate patient selection, optimal timing of intervention, and rational combination approaches aimed at sustaining repigmentation and reducing relapse risk. Collectively, these developments support the emerging role of JAK-directed therapy as a significant advancement in the management of vitiligo.

PMID:
42706213
Bibliographic data and abstract were imported from PubMed on 08 Sep 2026.

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