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首页> 外文期刊>Journal of neurovirology >NKG2D contributes to efficient clearance of picornavirus from the acutely infected murine brain.
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NKG2D contributes to efficient clearance of picornavirus from the acutely infected murine brain.

机译:NKG2D有助于从急性感染的鼠脑中有效清除小核糖核酸病毒。

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摘要

Activated murine cytotoxic T cells express the NKG2D natural cytotoxicity receptor. This receptor recognizes major histocompatibility complex (MHC) class I-like molecules expressed on the surface of infected cells and serves to augment T cell-mediated cytotoxicity. The role of NKG2D-mediated augmentation in the clearance of central nervous system viral infections has not been explored. Using the Theiler's murine encephalomyelitis virus model, the authors found that NKG2D-positive CD8+ cytotoxic T cells enter the brain, that NKG2D ligands are expressed in the brain during acute infection, and that interruption of NKG2D ligand recognition via treatment with a function-blocking antibody attenuates the efficacy of viral clearance from the central nervous system.
机译:活化的鼠细胞毒性T细胞表达NKG2D天然细胞毒性受体。该受体识别在感染细胞表面表达的主要组织相容性复合物(MHC)I类分子,并增强T细胞介导的细胞毒性。 NKG2D介导的增强在清除中枢神经系统病毒感染中的作用尚未探索。使用泰勒氏鼠脑脊髓炎病毒模型,作者发现NKG2D阳性CD8 +细胞毒性T细胞进入大脑,在急性感染期间NKG2D配体在大脑中表达,并且通过使用功能阻断抗体治疗破坏NKG2D配体识别减弱了从中枢神经系统清除病毒的功效。

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