Host-pathogen interaction in the tissue environment during Plasmodium blood-stage infection
Host-pathogen interaction in the tissue environment during Plasmodium blood-stage infection
复制标题
疟原虫血期感染期间组织环境中宿主与病原体的相互作用
DOI：
10.1111/pim.12763
复制
发表时间：
2021
期刊：
影响因子：
2.2
通讯作者：
S. Inoue
中科院分区：
文献类型：
--
作者：
K. Yui;S. Inoue
人类感染疟疾是在被具有传染性的按蚊叮咬后发生的。在最初的肝脏阶段感染后，寄生虫转化为裂殖子，感染红细胞（RBC）。然后在血液阶段感染期间发生反复RBC感染，而患者会出现各种疟疾症状。这种系统性感染引起保护性免疫反应，但过度的反应有时对宿主有害。由于寄生虫在此阶段仅感染RBC及其直接前体，因此直接的寄生虫-宿主相互作用主要发生在血管内皮衬里包围的环境中。脾脏是免疫系统遇到受感染的红细胞，引起免疫反应的主要器官。疟原虫在红细胞内表达PfEMP-1和RIFIN等蛋白质，这些蛋白质被转运到红细胞表面，通过将自身隔离在外周血管系统中避开脾脏或通过抑制性受体直接抑制免疫细胞来逃避免疫攻击。宿主细胞产生的调节性细胞因子IL-10和IL-27限制了过度的免疫反应，避免了组织损伤。通过宿主-寄生虫相互作用调节保护性和抑制性免疫应答，从而导致慢性疟原虫感染。在这篇综述中，我们讨论了潜在的相互作用机制，制定有效的战略，以对抗疟疾。
Human malarial infection occurs after an infectiousAnophelesmosquito bites. Following the initial liver‐stage infection, parasites transform into merozoites, infecting red blood cells (RBCs). Repeated RBC infection then occurs during the blood‐stage infection, while patients experience various malarial symptoms. Protective immune responses are elicited by this systemic infection, but excessive responses are sometimes harmful for hosts. As parasites infect only RBCs and their immediate precursors during this stage, direct parasite‐host interactions occur primarily in the environment surrounded by endothelial lining of blood vessels. The spleen is the major organ where the immune system encounters infected RBCs, causing immunological responses. Its tissue structure is markedly altered during malarial infection in mice and humans.Plasmodium falciparumparasites inside RBCs express proteins, such as PfEMP‐1 and RIFIN, transported to the RBC surfaces in order to evade immunological attack by sequestering themselves in the peripheral vasculature avoiding spleen or by direct immune cell inhibition through inhibitory receptors. Host cell production of regulatory cytokines IL‐10 and IL‐27 limits excessive immune responses, avoiding tissue damage. The regulation of the protective and inhibitory immune responses through host‐parasite interactions allows chronicPlasmodiuminfection. In this review, we discuss underlying interaction mechanisms relevant for developing effective strategies against malaria.