Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (ASTAR), Singapore, Singapore.
Department of Microbiology and Immunology, University of Otago, Dunedin, New Zealand.
Front Immunol. 2019 Jun 27;10:1444. doi: 10.3389/fimmu.2019.01444. eCollection 2019.
After a successful invasion, malaria parasite extensively remodels the infected erythrocyte cellular architecture, conferring cytoadhesive properties to the infected erythrocytes. Cytoadherence plays a central role in the parasite's immune-escape mechanism, at the same time contributing to the pathogenesis of severe falciparum malaria. In this review, we discuss the cytoadhesive interactions between infected erythrocytes and various host cell types, and how these events are linked to malaria pathogenesis. We also highlight the limitations faced by studies attempting to correlate diversity in parasite ligands and host receptors with the development of severe malaria.
疟原虫在成功入侵后，会广泛重塑感染的红细胞的细胞结构，使感染的红细胞具有细胞黏附特性。细胞黏附在寄生虫的免疫逃避机制中起着核心作用，同时也导致严重疟疾的发病机制。在这篇综述中，我们讨论了感染的红细胞与各种宿主细胞类型之间的细胞黏附相互作用，以及这些事件如何与疟疾发病机制相关联。我们还强调了试图将寄生虫配体和宿主受体的多样性与严重疟疾的发展相关联的研究所面临的局限性。
