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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Blood-stage Plasmodium Infection Induces Cd8~+ T Lymphocytes To Parasite-expressed Antigens, Largely Regulated By Cd8α~+ Dendritic Cells
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Blood-stage Plasmodium Infection Induces Cd8~+ T Lymphocytes To Parasite-expressed Antigens, Largely Regulated By Cd8α~+ Dendritic Cells

机译：血期疟原虫感染诱导Cd8〜+ T淋巴细胞寄生虫表达的抗原，很大程度上由Cd8α〜+树突状细胞调节。

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摘要

Although CD8~+ T cells do not contribute to protection against the blood stage of Plasmodium infection, there is mounting evidence that they are principal mediators of murine experimental cerebral malaria (ECM). At present, there is no direct evidence that the CD8~+ T cells mediating ECM are parasite-specific or, for that matter, whether parasite-specific CD8~+ T cells are generated in response to blood-stage infection. To resolve this and to define the cellular requirements for such priming, we generated transgenic P. berghei parasites expressing model T cell epitopes. This approach was necessary as MHC class I-restricted antigens to blood-stage infection have not been defined. Here, we show that blood-stage infection leads to parasite-specific CD8~+ and CD4~+ T cell responses. Furthermore, we show that P. berghei-expressed antigens are cross-presented by the CD8α~+ subset of dendritic cells (DC), and that this induces pathogen-specific cytotoxic T lymphocytes (CTL) capable of lysing cells presenting antigens expressed by blood-stage parasites. Finally, using three different experimental approaches, we provide evidence that CTL specific for parasite-expressed antigens contribute to ECM.
机译：尽管CD8〜+ T细胞无助于抵抗疟原虫感染的血液阶段，但越来越多的证据表明它们是鼠实验性脑疟疾（ECM）的主要介体。目前，尚无直接证据表明介导ECM的CD8 + T细胞是寄生虫特异性的，或者就此而言，是否响应血液阶段感染而产生了寄生虫特异性CD8 + T细胞。为解决此问题并定义此类引发的细胞要求，我们生成了表达模型T细胞表位的转基因伯氏疟原虫。该方法是必要的，因为尚未定义针对MHC I类限制的血阶段感染抗原。在这里，我们表明血液阶段感染导致寄生虫特异性CD8〜+和CD4〜+ T细胞反应。此外，我们表明，伯氏疟原虫表达的抗原是由树突状细胞（DC）的CD8α〜+亚型交叉呈递的，并且这诱导了病原体特异性的细胞毒性T淋巴细胞（CTL），其能够裂解呈递血液表达抗原的细胞阶段的寄生虫。最后，使用三种不同的实验方法，我们提供了证明寄生虫表达的抗原特异的CTL有助于ECM。

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