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Leflunomide-Mediated Immunomodulation Inhibits Lesion Progression in a Vitiligo Mouse Model.

Fang Miao1, Xiaohui Li1, Liang Zhao1

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Leflunomide (LEF) effectively treats vitiligo by inhibiting CD8+ T cells and restoring immune balance. This immunomodulator reduces depigmentation and shifts cytokine profiles, offering a promising therapeutic strategy.

Keywords:
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Area of Science:

  • Immunology
  • Dermatology
  • Pharmacology

Background:

  • Vitiligo pathogenesis involves autoimmune CD8+ T cell destruction of melanocytes.
  • Inhibiting CD8+ T cell functions and skin migration presents a viable therapeutic approach for vitiligo.

Purpose of the Study:

  • To investigate the therapeutic potential of leflunomide (LEF) in a mouse model of vitiligo.
  • To evaluate LEF's effects on T cell regulation, chemokine expression, and cytokine profiles in vitiligo.

Main Methods:

  • Utilized a tyrosine-related protein (TRP) 2-180-induced vitiligo mouse model.
  • Employed flow cytometry, immunofluorescence, ELISA, and histopathological analyses.
  • Systematically assessed LEF's impact on immune cell infiltration and molecular signaling.

Main Results:

  • LEF treatment (20 mg/kg/day) significantly reduced depigmentation and CD8+ T cell infiltration.
  • LEF suppressed the IFN-γ-driven expression of CXCL9 and CXCL10.
  • LEF restored CD4+/CD8+ T cell homeostasis and rebalanced pro- and anti-inflammatory cytokines, promoting a Th1 to Th2 shift.

Conclusions:

  • Leflunomide acts as an effective immunomodulator for vitiligo.
  • LEF disrupts the IFN-γ-CXCL9/10 axis, crucial in vitiligo progression.
  • LEF offers a promising repurposing strategy for halting vitiligo by re-establishing immune balance.