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.
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。
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