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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Differential tumor necrosis factor receptor 2-mediated editing of virus-specific CD8(+) effector T cells
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Differential tumor necrosis factor receptor 2-mediated editing of virus-specific CD8(+) effector T cells

机译：差异性肿瘤坏死因子受体2介导的病毒特异性CD8（+）效应T细胞的编辑

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Much of the CD8(+) T cell response in H2(b) mice with influenza pneumonia is directed at the nucleoprotein(366-374) (NP366) and acid polymerase(224-233) (PA(224)) peptides presented by the H2D(b) MHC class I glycoprotein. These (DNP366-)-N-b and D(b)PA(224-)specific T cell populations are readily analyzed by staining with tetrameric complexes of MHC+ peptide (tetramers) or by cytokine production subsequent to in vitro stimulation with the cognate peptides. The D(b)PA(224)(-) specific CD8(+) effector T cells make more tumor necrosis factor (TNF) alpha than the comparable CD8(+)D(b)NP(366)(+) set, a difference reflected in the greater sensitivity of the CD8(+)D(b)PA(224)(+) population to TNF receptor (TNFR) 2-mediated apoptosis under conditions of in vitro culture. Freshly isolated CD8(+)D(b)NP(366)(+) and CD8(+)D(b)PA(224)(+) T cells from influenza-infected TNFR2(-/-) mice produce higher levels of IFN-gamma and TNF-alpha after in vitro stimulation with peptide, although the avidity of the T cell receptor-epitope interaction does not change. Increased numbers of both CD8(+)D(b)PA(224)(+) and CD8(+)D(b)NP(366)(+) T cells were recovered from the lungs (but not the spleens) of secondarily challenged TNFR2(-/-) mite, a pattern that correlates with the profiles of TNFR expression in the TNFR2(+/+) controls. Thus, it seems that TNFR2-mediated editing of nfluenza-specific CD8(+) T cells functions to limit the numbers of effectors that have localized to the site of pathology in the lung but does not modify the size of the less activated responder T cell populations in the spleen. Therefore, the massive difference in magnitude for the secondary, although not the primary, response to these (DNP366-)-N-b and D(b)PA(224) epitopes cannot be considered to reflect differential TNFR2-mediated T cell editing. [References: 51]
机译：H2（b）流感病毒性肺炎小鼠中的大部分CD8（+）T细胞应答都针对核蛋白（366-374）（NP366）和酸性聚合酶（224-233）（PA（224））肽， H2D（b）MHC I类糖蛋白。这些（DNP366-）-N-b和D（b）PA（224-）特异性T细胞群体可通过用MHC +肽的四聚体复合物（四聚体）染色或在通过同源肽体外刺激后产生细胞因子来容易地进行分析。 D（b）PA（224）（-）特异的CD8（+）效应T细胞比可比较的CD8（+）D（b）NP（366）（+）集产生更多的肿瘤坏死因子（TNF）α，差异反映在体外培养条件下，CD8（+）D（b）PA（224）（+）群体对TNF受体（TNFR）2介导的细胞凋亡的敏感性更高。从流感感染的TNFR2（-/-）小鼠新鲜分离的CD8（+）D（b）NP（366）（+）和CD8（+）D（b）PA（224）（+）T细胞产生更高水平的尽管T细胞受体-表位相互作用的亲和力没有改变，但在体外用肽刺激后，IFN-γ和TNF-α却没有改变。其次，从肺（但不是脾脏）中回收到增加的CD8（+）D（b）PA（224）（+）和CD8（+）D（b）NP（366）（+）T细胞数量挑战TNFR2（-/-）螨，该模式与TNFR2（+ / +）对照中TNFR表达的特征相关。因此，似乎由TNFR2介导的流感特异性CD8（+）T细胞的编辑功能是限制已经定位于肺部病理部位的效应子的数量，但不会改变反应性较弱的T细胞的大小脾脏中的人口。因此，对于这些（DNP366-）-N-b和D（b）PA（224）表位的次要反应（而非主要反应），其幅度的巨大差异不能视为反映差异性TNFR2介导的T细胞编辑。 [参考：51]

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