On the pathogenic role of brain-sequestered αβ CD8+ T cells in experimental cerebral malarial
On the pathogenic role of brain-sequestered αβ CD8+ T cells in experimental cerebral malarial
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DOI：
10.4049/jimmunol.169.11.6369
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发表时间：
2002-12-01
影响因子：
4.4
通讯作者：
Rénia, L
中科院分区：
文献类型：
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作者：
Belnoue, E;Kayibanda, M;Rénia, L
脑型疟疾（CM）在感染恶性疟原虫的人中的一小部分中发展，并且占由于这种寄生虫引起的死亡的相当大的比例。实际的致病机制仍然知之甚少，在人类实验CM的调查是不道德的。使用已建立的伯氏疟原虫-小鼠CM模型，我们研究了宿主免疫细胞在病理部位（脑）的作用。在这项研究中，我们报告了细胞的详细定量和表征，这些细胞迁移并隔离到CM小鼠的大脑中。我们证明，当神经系统症状出现时，在大脑中隔离的CD 8（+）α T细胞是CM死亡率的原因。这些观察结果表明了一种机制，它统一了人类的不同观察结果。
Cerebral malaria (CM) develops in a small proportion of persons infected with Plasmodium falciparum and accounts for a substantial proportion of the mortality due to this parasite. The actual pathogenic mechanisms are still poorly understood, and in humans investigations of experimental CM are unethical. Using an established Plasmodium berghei-mouse CM model, we have investigated the role of host immune cells at the pathological site, the brain. We report in this study the detailed quantification and characterization of cells, which migrated and sequestered to the brain of mice with CM. We demonstrated that CD8(+) alphabeta T cells, which sequester in the brain at the time when neurological symptoms appear, were responsible for CM mortality. These observations suggest a mechanism which unifies disparate observations in humans.