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<p>Systemic lupus erythematosus (SLE) is an autoimmune disease driven by autoantibody production. Lupus nephritis (LN), a severe SLE complication, is primarily caused by renal autoantibodies. Long-lived plasma cells (LLPCs), the main producers of these autoantibodies, are especially elevated in the kidney of LN patients, particularly in refractory or recurrent cases. However, the cause of increased LLPCs in LN kidneys remains unknown. This study uses an LN mouse model and combines single-cell RNA sequencing with spatial transcriptomics, finding that kidney-resident Cxcl9<sup>high</sup> macrophages and their secreted chemokine Cxcl9 significantly rise with disease progression. This increase in Cxcl9 attracts Cxcr3+ plasmablasts in peripheral blood into the kidneys, where they differentiate into LLPCs and produce autoantibodies. Based on these findings, this study suggests that Cxcl9<sup>high</sup> macrophages are the inducing factor causing the increase of LLPCs in LN kidneys and may be a potential therapeutic target for LN.</p><p></p>

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Cxcl9high macrophages recruit circulating Cxcr3+ plasmablasts into kidneys to promote pathogenesis of lupus nephritis mice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月9日

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  • Jing Zhao,
  • Xinlong Bai,
  • Cheng Zhou,
  • Qing Ouyang,
  • Yingjie Zhang,
  • Xiao Zhang,
  • Xumin Zheng,
  • Chaofan Li,
  • Wanjun Shen,
  • Qinggang Li,
  • Guangyan Cai,
  • Xiangmei Chen,
  • Ping Li,
  • Xue-Yuan Bai

摘要

Systemic lupus erythematosus (SLE) is an autoimmune disease driven by autoantibody production. Lupus nephritis (LN), a severe SLE complication, is primarily caused by renal autoantibodies. Long-lived plasma cells (LLPCs), the main producers of these autoantibodies, are especially elevated in the kidney of LN patients, particularly in refractory or recurrent cases. However, the cause of increased LLPCs in LN kidneys remains unknown. This study uses an LN mouse model and combines single-cell RNA sequencing with spatial transcriptomics, finding that kidney-resident Cxcl9high macrophages and their secreted chemokine Cxcl9 significantly rise with disease progression. This increase in Cxcl9 attracts Cxcr3+ plasmablasts in peripheral blood into the kidneys, where they differentiate into LLPCs and produce autoantibodies. Based on these findings, this study suggests that Cxcl9high macrophages are the inducing factor causing the increase of LLPCs in LN kidneys and may be a potential therapeutic target for LN.