Mosquito-transmitted Plasmodium falciparum infection can cause human cerebral malaria (HCM) with high mortality rates. The abundance of infected red blood cells that accumulate in the cerebral vasculature of patients has led to the belief that these brain-sequestered cells solely cause pathogenesis. However, animal models suggest that CD8+ T cells migrate to and accumulate in the brain, directly contributing to experimental cerebral malaria (ECM) mortality. In this issue of the JCI, Riggle et al. explored the brain vasculature from 34 children who died from HCM or other causes and frequently found CD3+ CD8+ T cells in contact with endothelial cells. Further, the authors show that coinfection with HIV enhanced such CD3+ CD8+ T cell luminal distribution. These findings suggest that the mouse model for cerebral malaria may accurately reflect human disease pathology. This study sheds new light on the mechanisms behind blood-brain barrier breakdown in this complicated neurological disease and opens up alternative approaches for treatment.

中文翻译：

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CD8 + T细胞和人脑疟疾：不断变化的认识。

蚊子传播的恶性疟原虫感染可导致高死亡率的人脑疟疾。在患者的脑血管中积累的大量受感染的红细胞导致人们相信这些脑隔离细胞仅会引起发病。但是，动物模型表明CD8 + T细胞迁移到大脑并在大脑中积累，直接导致实验性脑疟疾（ECM）死亡。在本期JCI中，Riggle等人。探索了34名因HCM或其他原因死亡的儿童的脑血管，并经常发现CD3 + CD8 + T细胞与内皮细胞接触。此外，作者表明，与HIV的共感染增强了CD3 + CD8 + T细胞的管腔分布。这些发现表明，脑疟疾的小鼠模型可以准确反映人类疾病的病理学。这项研究为这种复杂的神经疾病中血脑屏障破坏的机制提供了新的思路，并开辟了替代治疗方法。