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BRIEF RESEARCH REPORT article

Front. Med.
Sec. Dermatology
Volume 12 - 2025 | doi: 10.3389/fmed.2025.1466996
This article is part of the Research Topic Exploring Pigmentary Disorders: Pathogenesis to Treatment View all articles

Local Sympathetic Nerve Depletion Does Not Alter Vitiligo Progression in a Mouse Model

Provisionally accepted
Zhichao Hu Zhichao Hu 1,2*Ting Chen Ting Chen 1,2,3*Daoming Chen Daoming Chen 2*
  • 1 Graduate School, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
  • 2 National Institute of Biological Sciences (NIBS), Beijing, Beijing Municipality, China
  • 3 Tsinghua Institute of Multidisciplinary Biomedical Research, Tsinghua University, Beijing, Beijing Municipality, China

The final, formatted version of the article will be published soon.

    Vitiligo, an autoimmune skin disorder characterized by melanocyte loss, has long been associated with sympathetic nervous system activity. Clinical observations have suggested links between psychological stress, sympathetic activation, and vitiligo progression. However, direct experimental evidence for the role of sympathetic nerves in vitiligo development has been lacking.Herein, we employed 6-hydroxydopamine (6-OHDA) to induce sympathetic nerve depletion in mice before vitiligo induction. Sympathetic nerve ablation was confirmed through immunofluorescent staining of tyrosine hydroxylase. Vitiligo progression was assessed by quantifying epidermal melanocytes and CD8+ T cells using whole-mount immunofluorescence staining. The loss of melanocytes and infiltration of CD8+ T cells in vitiligo lesions were comparable between sympathectomized and control mice. Overall, our study suggested that previously observed associations between sympathetic nervous system activity and vitiligo may be concomitant effects rather than causative factors, challenging long-held clinical hypotheses.

    Keywords: autoimmune disease, skin disease, Vitiligo, sympathetic nerve, melanocyte, CD8+ T cell

    Received: 19 Jul 2024; Accepted: 15 Jan 2025.

    Copyright: © 2025 Hu, Chen and Chen. 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:
    Zhichao Hu, Graduate School, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China
    Ting Chen, National Institute of Biological Sciences (NIBS), Beijing, 102206, Beijing Municipality, China
    Daoming Chen, National Institute of Biological Sciences (NIBS), Beijing, 102206, Beijing Municipality, China

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