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首页> 外文期刊>Experimental Gerontology >Intrinsic defects in CD8 T cells with aging contribute to impaired primary antiviral responses
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Intrinsic defects in CD8 T cells with aging contribute to impaired primary antiviral responses

机译：CD8 T细胞的内在缺陷会随着衰老而导致原发性抗病毒反应受损

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摘要

Aging is associated with altered immune responses, particularly with a diminished CD8 T cell response. Although both intrinsic and extrinsic factors are hypothesized to impact this decreased T cell response, the direct evidence of an intrinsic deficiency in virus-specific CD8 T cells is limited. In this study, a TCR transgenic (Tg) P14 mouse model was utilized to compare the activation and proliferation of the Tg CD8 T cells of young and aged P14 mice upon stimulation with antigen or infection with virus. The proliferation of purified Tg CD8 T cells of aged mice was significantly lower than that of young mice when cultured in vitro with both the LCMV specific peptide and antigen presenting cells from young wild type mice. In addition, expression of the activation markers, CD69, CD25, and CD44, was delayed on Tg T cells of aged mice after stimulation. Importantly, while adoptive transfer of purified Tg CD8 T cells of young or aged mice into young wild type mice resulted in expansion of the Tg CD8 T cells of both ages after LCMV infection, the expansion of the Tg T cells from aged mice was significantly decreased compared with that of the Tg T cells from young mice. However, while the number of IFN-γ secreting Tg CD8 T cells from aged mice was significantly decreased compared to that of young mice, the percentages of Tg CD8 T cells producing IFN-γ were similar in young and aged mice, demonstrating that proliferation, but not function, of the Tg CD8 T cells of aged mice was impaired. Importantly, chronological age alone was not sufficient to predict an altered proliferative response; rather, expression of high levels of CD44 on CD8 T cells of aged mice reflected a decreased proliferative response. These results reveal that alterations intrinsic to CD8 T cells can contribute to the age-associated defects in the primary CD8 T cell response during viral infection.
机译：衰老与免疫反应改变有关，特别是与CD8 T细胞反应减少有关。尽管假设内在因素和外在因素均会影响这种降低的T细胞反应，但病毒特异性CD8 T细胞内在缺乏的直接证据是有限的。在这项研究中，TCR转基因（Tg）P14小鼠模型用于比较抗原刺激或病毒感染后年轻和老年P14小鼠Tg CD8 T细胞的活化和增殖。当与来自幼龄野生型小鼠的LCMV特异性肽和抗原呈递细胞体外培养时，老年小鼠的纯化的Tg CD8 T细胞的增殖显着低于幼年小鼠的增殖。此外，刺激后，衰老小鼠的Tg T细胞上的激活标记CD69，CD25和CD44的表达被延迟。重要的是，LCMV感染后，尽管将成年或成年小鼠的纯化Tg CD8 T细胞过继转移至成年野生型小鼠中导致两个年龄的Tg CD8 T细胞扩增，但衰老小鼠Tg T细胞的扩增却显着减少与年轻小鼠的Tg T细胞相比。但是，虽然与年轻小鼠相比，老年小鼠分泌IFN-γ的Tg CD8 T细胞的数量明显减少，但幼龄和老年小鼠中产生IFN-γ的Tg CD8 T细胞的百分比却相似，这表明增殖，而非衰老小鼠的Tg CD8 T细胞受损。重要的是，仅按年龄顺序还不足以预测增生反应的改变。相反，衰老小鼠的CD8 T细胞上高水平的CD44表达反映了增殖反应的降低。这些结果表明，CD8 T细胞固有的改变可导致病毒感染过程中主要CD8 T细胞反应中与年龄相关的缺陷。

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