Review demonstrates targeted modulation of JAK-STAT signaling in vitiligo, highlighting improved repigmentation over conventional immunosuppression.
Key Points
To examine the role of dysregulated JAK-STAT signaling in vitiligo pathogenesis and evaluate the therapeutic efficacy of topical and systemic Janus kinase inhibitors.
Literature search conducted using PubMed/MEDLINE for studies published up to January 2026.
Analyzed the contribution of JAK-STAT-dependent pathways, IFN-γ-induced chemokines (CXCL9, CXCL10), cytotoxic CD8+ T cells, and tissue-resident memory T cells.
Evaluated clinical data on topical and systemic JAK inhibitors across melanocytes, keratinocytes, and immune cells.
Dysregulated JAK-STAT signaling mediates IFN-γ-induced chemokine production (CXCL9 and CXCL10) and cytotoxic CD8+ T-cell recruitment, driving autoimmune melanocyte destruction.
Janus kinase inhibitors achieve targeted immunosuppression across keratinocytes, melanocytes, and immune cells rather than broad systemic suppression.
Current clinical evidence supports both topical and systemic JAK inhibitors as effective repigmentation therapies, though long-term success requires strategies to address tissue-resident memory T cells and relapse risk.