MINI REVIEW article
Front. Immunol.
Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders
The role of JAK3 and TEC family kinases in vitiligo pathogenesis
Thierry Passeron 1,2
Julien Seneschal 3,4
Mauro Picardo 5
Leihong Xiang 6
Atsushi Tanemura 7
Aaron Winkler 8
Jean-Baptiste Telliez 8
Roni Adiri 9
1. University Côte d’Azur, Centre Hospitalier Universitaire Nice, Department of Dermatology, Nice, France
2. University Côte d’Azur, INSERM, U1065, C3M, Nice, France
3. CHU de Bordeaux, Department of Dermatology and Pediatric Dermatology, National Reference Center for Rare Skin Diseases, Hôpital Saint-André, UMR 5164, F-33000, Bordeaux, France
4. University Bordeaux, CNRS, Immuno ConcEpT, UMR 5164, F-33000, Bordeaux, France
5. Istituto Dermopatico Immacolata IDI, IRCCS, Rome, Italy
6. Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, China
7. Department of Dermatology Integrated Medicine, Osaka University Graduate School of Medicine, Osaka, Japan
8. Inflammation and Immunology Research Unit, Pfizer Inc., Cambridge, MA, United States
9. Pfizer Pharmaceutical Israel LTD, Herzliya Pituach, Israel
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Abstract
Vitiligo is an autoimmune disease characterized by the loss of skin pigmentation due to the loss of melanocytes. The pathogenesis of vitiligo is complex, involving multiple genetic factors, environmental triggers, oxidative stress, and autoimmunity against melanocytes. Stressed melanocytes release damage-associated molecular patterns which trigger increased activation of antigen presenting cells, leading to maturation and activation of CD8+ T-cells that respond to auto-melanocyte-specific antigens. Once recruited to melanocytes, cytotoxic CD8+ and CD4+ T-cells produce cytokines, including primarily the type 1 cytokine IFN-γ, but also IL-2, IL-15, and type 2-related cytokines. Cytokines bind to fibroblasts, melanocytes, and keratinocytes to induce a positive feedback loop of immune cell recruitment to lesions, immune cell activation, and melanocyte apoptosis. The JAK/STAT pathway and TEC family kinase signaling play key roles in vitiligo pathogenesis through chemokine production, reduction of melanocyte adhesion, and immune cell activation and disease maintenance. This review summarizes recent key advances in understanding how these pathways impact vitiligo pathogenesis and details the emergence of new targeted therapies for the treatment of vitiligo.
Summary
Keywords
Autoimmune disorder, cytokine, Disease pathogenesis, JAK3 (Janus kinase 3), JAK-STAT signaling pathway, targeted therapy, Tec familykinases, Vitiligo
Received
08 July 2025
Accepted
17 February 2026
Copyright
© 2026 Passeron, Seneschal, Picardo, Xiang, Tanemura, Winkler, Telliez and Adiri. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Thierry Passeron
Disclaimer
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