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<p>Antimalarial drug resistance poses a critical threat to global malaria control efforts. Despite the continuous development of novel antimalarial compounds, the emergence of drug resistance remains inevitable, highlighting the urgent need for paradigm-shifting therapeutic approaches. Here, we propose an innovative chimeric antigen receptor-macrophage (CAR-M) cell therapy that circumvents traditional small-molecule limitations by harnessing the innate phagocytic capacity of macrophages. This strategy exploits the specific adhesive interactions between <i>Plasmodium falciparum</i> erythrocyte membrane protein 1 (PfEMP1) and host receptors (CD36, ICAM-1/CD54, EPCR/CD201) to enable targeted recognition and elimination of infected erythrocytes. By engineering macrophages with chimeric antigen receptors directed against PfEMP1-binding domains, we establish a cell-based immunotherapy platform that provides sustained anti-parasitic activity independent of conventional drug susceptibility profiles. This approach represents a fundamental departure from chemical-based interventions by providing a potentially resistance-proof therapeutic modality for drug-resistant malaria.</p>

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CAR-macrophage therapy: a novel strategy to overcome antimalarial drug resistance by targeting PfEMP1-mediated adhesion

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月6日

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  • Daiqian Zhu,
  • Weijia Cheng,
  • Yao Zhang,
  • Huiyin Zhu,
  • Zhixin Liu,
  • Haimei Shi,
  • Qingfeng Zhang,
  • Jian Li

摘要

Antimalarial drug resistance poses a critical threat to global malaria control efforts. Despite the continuous development of novel antimalarial compounds, the emergence of drug resistance remains inevitable, highlighting the urgent need for paradigm-shifting therapeutic approaches. Here, we propose an innovative chimeric antigen receptor-macrophage (CAR-M) cell therapy that circumvents traditional small-molecule limitations by harnessing the innate phagocytic capacity of macrophages. This strategy exploits the specific adhesive interactions between Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) and host receptors (CD36, ICAM-1/CD54, EPCR/CD201) to enable targeted recognition and elimination of infected erythrocytes. By engineering macrophages with chimeric antigen receptors directed against PfEMP1-binding domains, we establish a cell-based immunotherapy platform that provides sustained anti-parasitic activity independent of conventional drug susceptibility profiles. This approach represents a fundamental departure from chemical-based interventions by providing a potentially resistance-proof therapeutic modality for drug-resistant malaria.