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Natural killer cell activation enhances immune pathology and promotes chronic infection by limiting CD8+ T-cell immunity.自然杀伤细胞的激活通过限制 CD8+T 细胞免疫来增强免疫病理并促进慢性感染。
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Natural killer cells act as rheostats modulating antiviral T cells.自然杀伤细胞充当调节抗病毒 T 细胞的变阻器。
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T cell exhaustion.T 细胞耗竭。
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Point mutation in the glycoprotein of lymphocytic choriomeningitis virus is necessary for receptor binding, dendritic cell infection, and long-term persistence.淋巴细胞脉络丛脑膜炎病毒糖蛋白中的点突变对于受体结合、树突状细胞感染和长期持续感染是必需的。
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Decoding arenavirus pathogenesis: essential roles for alpha-dystroglycan-virus interactions and the immune response.解析沙粒病毒发病机制：α- 肌营养不良聚糖与病毒相互作用和免疫应答的重要作用。
Virology. 2011 Mar 15;411(2):170-9. doi: 10.1016/j.virol.2010.11.023. Epub 2010 Dec 23.
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NKp46 and DNAM-1 NK-cell receptors drive the response to human cytomegalovirus-infected myeloid dendritic cells overcoming viral immune evasion strategies.NKp46 和 DNAM-1 NK 细胞受体驱动对人巨细胞病毒感染的髓样树突状细胞的反应，克服病毒的免疫逃避策略。
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Critical role of DNAX accessory molecule-1 (DNAM-1) in the development of acute graft-versus-host disease in mice.DNAX 辅助分子-1（DNAM-1）在小鼠急性移植物抗宿主病中的关键作用。
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Loss of DNAM-1 contributes to CD8+ T-cell exhaustion in chronic HIV-1 infection.DNAM-1 的缺失导致慢性 HIV-1 感染中 CD8+ T 细胞耗竭。
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9
DNAM-1 promotes activation of cytotoxic lymphocytes by nonprofessional antigen-presenting cells and tumors.DNAM-1可促进非专职抗原呈递细胞和肿瘤对细胞毒性淋巴细胞的激活。
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10
Characterization of the recognition and functional heterogeneity exhibited by cytokine-induced killer cell subsets against acute myeloid leukaemia target cell.细胞因子诱导的杀伤细胞亚群对急性髓系白血病靶细胞表现出的识别和功能异质性的特征分析。
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DNAM-1 缺陷小鼠中 TNF-α 和 IL-2 的 CD8 T 细胞缺陷延迟了持续性病毒感染的体内清除。

CD8 T cell defect of TNF-α and IL-2 in DNAM-1 deficient mice delays clearance in vivo of a persistent virus infection.

机构信息

Department of Immunology and Microbial Science, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.

出版信息

Virology. 2012 Aug 1;429(2):163-70. doi: 10.1016/j.virol.2012.04.006. Epub 2012 May 12.

DOI:10.1016/j.virol.2012.04.006
PMID:22579352
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3571684/
Abstract

DNAM-1 gene-deficient (-/-) mice take significantly longer to clear an acute and persistent LCMV infection in vivo than DNAM-1 +/+ mice. During acute LCMV priming, at the single cell level, DNAM-1 -/- mice made significantly less cytoplasmic CD8 TNF-α and IL-2 but not IFN-γ than their DNAM-1 +/+ counterparts. Restimulated immune memory CD8 T cells from DNAM-1 -/- and DNAM-1 +/+ mice were equivalent in cytolytic activity against LCMV-infected target cells but DNAM-1 -/- CD8 T cells had significant reductions in TNF-α and IL-2 that were associated on adoptive transfer with the inability to terminate the persistent viral infection.

摘要

DNAM-1 基因缺失（-/-）的小鼠在体内清除急性持续性 LCMV 感染的速度明显慢于 DNAM-1 +/+ 的小鼠。在急性 LCMV 启动阶段，在单细胞水平上，DNAM-1 -/- 的小鼠产生的细胞质 CD8 TNF-α 和 IL-2 明显少于其 DNAM-1 +/+ 的对应物，但 IFN-γ 没有差异。从 DNAM-1 -/- 和 DNAM-1 +/+ 的小鼠中重新刺激免疫记忆 CD8 T 细胞，其对 LCMV 感染靶细胞的细胞毒性活性相当，但 DNAM-1 -/- CD8 T 细胞中 TNF-α和 IL-2 的水平显著降低，这与不能终止持续性病毒感染有关。