近日，刊登在国际著名杂志《PLoS Pathogens》上的一篇研究报告中，来自加拿大麦克马斯特大学的研究者表示，我们机体的免疫系统并不会随着年龄的增长而关闭。这项研究揭示了一组特殊类别的免疫细胞，名为T细胞，在老年人机体中T细胞可以对病毒感染进行反应，而且T细胞的反应能力及活性与来自年轻人体内的T细胞活力一样。
研究者Jonathan Bramson表示，长期以来，人们一直认为老年人感染病毒细菌的风险较高，因为老年人缺少免疫细胞，但是实际上并不是这样，这样研究中，研究者研究发现，老年人依然有足够的免疫力来抵御病毒的感染。
文章中，研究者对年龄小于40的个体、41至59岁以及超过60岁的，感染三种不同病毒（包括西尼罗病毒）的个体进行研究，发现老年人一组同样也表现出了正常的免疫系统反应。抵御病毒的T细胞数量以及功能性的T细胞数量在三个研究群体中都是等同的。
研究者Bramson说，因此随着我们年龄增长，我们机体仍然可以对病毒产生较强的免疫反应，而且这种免疫反应能力与年轻时候是一样的。
本文的研究结果对于开发老年人专用的疫苗具有重要的指示意义。当然，针对于老年人的疫苗很难开发出来以引起机体免疫细胞的反应，这项研究或帮助解释流感疫苗有效保护效应的缺失。本文研究揭示了，疫苗可以被特异性地开发出来来产生T细胞免疫力，这或许可以更加有效地保护老年人。
这项研究由加拿大卫生研究院以及美国**卫生院提供资助。
The Polyfunctionality of Human Memory CD8+ T Cells Elicited by Acute and Chronic Virus Infections Is Not Influenced by Age
Alina Lelic1, Chris P. Verschoor1, Mario Ventresca2, Robin Parsons1, Carole Evelegh1, Dawn Bowdish1, Michael R. Betts3, Mark B. Loeb1, Jonathan L. Bramson1*
As humans age, they experience a progressive loss of thymic function and a corresponding shift in the makeup of the circulating CD8+ T cell population from na?ve to memory phenotype. These alterations are believed to result in impaired CD8+ T cell responses in older individuals; however, evidence that these global changes impact virus-specific CD8+ T cell immunity in the elderly is lacking. To gain further insight into the functionality of virus-specific CD8+ T cells in older individuals, we interrogated a cohort of individuals who were acutely infected with West Nile virus (WNV) and chronically infected with Epstein Barr virus (EBV) and Cytomegalovirus (CMV). The cohort was stratified into young (<40 yrs), middle-aged (41–59 yrs) and aged (>60 yrs) groups. In the aged cohort, the CD8+ T cell compartment displayed a marked reduction in the frequency of na?ve CD8+ T cells and increased frequencies of CD8+ T cells that expressed CD57 and lacked CD28, as previously described. However, we did not observe an influence of age on either the frequency of virus-specific CD8+ T cells within the circulating pool nor their functionality (based on the production of IFNγ, TNFα, IL2, Granzyme B, Perforin and mobilization of CD107a). We did note that CD8+ T cells specific for WNV, CMV or EBV displayed distinct functional profiles, but these differences were unrelated to age. Collectively, these data fail to support the hypothesis that immunosenescence leads to defective CD8+ T cell immunity and suggest that it should be possible to develop CD8+ T cell vaccines to protect aged individuals from infections with novel emerging viruses.
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