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<p>Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex etiology involving both innate and adaptive immune dysregulation. Among several perturbed signaling pathways, decreased ERK activity in CD4⁺ T-cells has been linked to DNA hypomethylation and aberrant gene expression in SLE. Mebendazole (MBZ), an anti-helminthic drug with a well-established safety profile, has shown immunomodulatory effects in preclinical studies, including activation of the MEK/ERK pathway and inhibition of MAPK14 (p38), a known driver of inflammation. To evaluate the therapeutic potential of MBZ in SLE, we tested its efficacy in NZBxNZWF1 mice, a spontaneous and well-characterized SLE model. MBZ treatment resulted in reduced proteinuria, lower anti-dsDNA antibody levels, and diminished glomerular IgG deposition, both in preventive and therapeutic settings. Exploratory in vitro data suggest that MBZ may also influence ERK signaling in B cells, while the mechanistic basis of these effects remains to be clarified. Our findings demonstrate robust phenotypic improvements and support further investigation of MBZ as a repositioned candidate for SLE. </p>

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Efficacy of mebendazole in the spontaneous NZBxNZWF1 animal model of systemic lupus erythematosus

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月12日

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  • M. L. Eloranta,
  • P. Nygren,
  • R. Larsson,
  • A. Loskog,
  • N. Woodworth,
  • M. Hultqvist,
  • Richard Svensson,
  • Ylva Gravenfors,
  • L. Rönnblom,
  • Mårten Fryknäs

摘要

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex etiology involving both innate and adaptive immune dysregulation. Among several perturbed signaling pathways, decreased ERK activity in CD4⁺ T-cells has been linked to DNA hypomethylation and aberrant gene expression in SLE. Mebendazole (MBZ), an anti-helminthic drug with a well-established safety profile, has shown immunomodulatory effects in preclinical studies, including activation of the MEK/ERK pathway and inhibition of MAPK14 (p38), a known driver of inflammation. To evaluate the therapeutic potential of MBZ in SLE, we tested its efficacy in NZBxNZWF1 mice, a spontaneous and well-characterized SLE model. MBZ treatment resulted in reduced proteinuria, lower anti-dsDNA antibody levels, and diminished glomerular IgG deposition, both in preventive and therapeutic settings. Exploratory in vitro data suggest that MBZ may also influence ERK signaling in B cells, while the mechanistic basis of these effects remains to be clarified. Our findings demonstrate robust phenotypic improvements and support further investigation of MBZ as a repositioned candidate for SLE.