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<p>Renal ischemia–reperfusion injury (IRI) is a major cause of acute kidney injury. It occurs in diverse clinical settings, including kidney transplantation, cardiac surgery, traumatic shock, and other conditions associated with transient renal hypoperfusion. The pathogenesis of renal IRI involves mitochondrial dysfunction, oxidative stress, ionic imbalance, endothelial activation, and sterile inflammation. Increasing evidence indicates that complement activation and immune cell infiltration are central amplifiers of renal IRI. Complement activation products, especially C3a and C5a, interact with C3aR and C5aR1 on tubular epithelial cells and immune cells, thereby promoting leukocyte recruitment, antigen-presenting cell activation, macrophage polarization, and T cell responses. Infiltrating neutrophils, macrophages, dendritic cells (DCs), natural killer (NK) cells, T cells, and B cells further aggravate tissue injury through cytokine release, oxidative burst, cytotoxicity, and crosstalk with complement pathways. This review summarizes the cellular and molecular mechanisms linking complement activation to immune cell responses in renal IRI and discusses potential regulatory strategies targeting the complement–immune axis.</p>

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Complement-immune cell crosstalk: shaping the immune landscape and regulatory strategies in renal ischemia-reperfusion injury

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月15日

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  • Xiaochuan Gong,
  • Han Zhu,
  • Zhengdao Liu,
  • Junjun Le,
  • Jiayu Zhao,
  • Yongjia Wan,
  • Mingzhou Li,
  • Jingjie Li,
  • Shulian Chen,
  • Bo Wang,
  • Guobiao Liang

摘要

Renal ischemia–reperfusion injury (IRI) is a major cause of acute kidney injury. It occurs in diverse clinical settings, including kidney transplantation, cardiac surgery, traumatic shock, and other conditions associated with transient renal hypoperfusion. The pathogenesis of renal IRI involves mitochondrial dysfunction, oxidative stress, ionic imbalance, endothelial activation, and sterile inflammation. Increasing evidence indicates that complement activation and immune cell infiltration are central amplifiers of renal IRI. Complement activation products, especially C3a and C5a, interact with C3aR and C5aR1 on tubular epithelial cells and immune cells, thereby promoting leukocyte recruitment, antigen-presenting cell activation, macrophage polarization, and T cell responses. Infiltrating neutrophils, macrophages, dendritic cells (DCs), natural killer (NK) cells, T cells, and B cells further aggravate tissue injury through cytokine release, oxidative burst, cytotoxicity, and crosstalk with complement pathways. This review summarizes the cellular and molecular mechanisms linking complement activation to immune cell responses in renal IRI and discusses potential regulatory strategies targeting the complement–immune axis.