Deb Chandra, Howe Charles L
Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA.
J Neurovirol. 2008 May;14(3):261-6. doi: 10.1080/13550280802105002.
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.
活化的小鼠细胞毒性T细胞表达NKG2D天然细胞毒性受体。该受体识别感染细胞表面表达的主要组织相容性复合体(MHC)I类样分子,并增强T细胞介导的细胞毒性。NKG2D介导的增强作用在中枢神经系统病毒感染清除中的作用尚未得到研究。利用泰勒氏小鼠脑脊髓炎病毒模型,作者发现NKG2D阳性的CD8 +细胞毒性T细胞进入大脑,在急性感染期间大脑中表达NKG2D配体,并且通过用功能阻断抗体治疗中断NKG2D配体识别会减弱从中枢神经系统清除病毒的功效。