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<p>Toll-like receptors (TLRs) play a pivotal role in the pathogenesis of systemic lupus erythematosus (SLE) by regulating the activation and differentiation of immune cells. Oleic acid (OA), the predominant monounsaturated fatty acid found in adipose tissue, is known to regulate various biological processes. However, the regulatory role of OA in TLR signaling pathways activation and SLE pathogenesis remains unclear. In this study, we reveal that OA treatment significantly alleviates symptoms in both MRL/<i>lpr</i> mice and imiquimod (IMQ)-induced lupus model mice, as evidenced by reduced splenomegaly, decreased anti-dsDNA antibody levels, ameliorated renal pathological damage, and diminished glomerular deposits of IgG and IgM. Notably, OA treatment not only suppresses the activation of immune cells, including B cells, macrophages, dendritic cells, and T cells, but also inhibits the differentiation of B cells and T cells in vivo. Importantly, OA effectively inhibits TLRs-mediated activation of immune cells by blocking the MAPK pathway and NF-κB pathway. Mechanistically, OA promotes IL-10 expression in B cells by activating STAT3, and IL-10 can significantly inhibit the activation of TLR pathways. Collectively, our findings reveal that OA mitigates lupus pathogenesis by targeting TLR pathways through the STAT3/IL-10 axis, indicating that OA may be a promising treatment candidate for SLE.</p>

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Oleic acid alleviates the pathogenesis of lupus by suppressing the activation of TLR signaling pathways through the STAT3/IL-10 axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月5日

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  • Yuxin Hu,
  • Yucai Xiao,
  • Yangzhe Gao,
  • Zhengyi Zhang,
  • Tianqi Zhao,
  • Shuo Zhao,
  • Jiakun Liu,
  • Huabao Xiong,
  • Yonghong Yang,
  • Guanjun Dong,
  • Lu Yu

摘要

Toll-like receptors (TLRs) play a pivotal role in the pathogenesis of systemic lupus erythematosus (SLE) by regulating the activation and differentiation of immune cells. Oleic acid (OA), the predominant monounsaturated fatty acid found in adipose tissue, is known to regulate various biological processes. However, the regulatory role of OA in TLR signaling pathways activation and SLE pathogenesis remains unclear. In this study, we reveal that OA treatment significantly alleviates symptoms in both MRL/lpr mice and imiquimod (IMQ)-induced lupus model mice, as evidenced by reduced splenomegaly, decreased anti-dsDNA antibody levels, ameliorated renal pathological damage, and diminished glomerular deposits of IgG and IgM. Notably, OA treatment not only suppresses the activation of immune cells, including B cells, macrophages, dendritic cells, and T cells, but also inhibits the differentiation of B cells and T cells in vivo. Importantly, OA effectively inhibits TLRs-mediated activation of immune cells by blocking the MAPK pathway and NF-κB pathway. Mechanistically, OA promotes IL-10 expression in B cells by activating STAT3, and IL-10 can significantly inhibit the activation of TLR pathways. Collectively, our findings reveal that OA mitigates lupus pathogenesis by targeting TLR pathways through the STAT3/IL-10 axis, indicating that OA may be a promising treatment candidate for SLE.