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　　近日，刊登在國際著(zhù)名雜志《PLoS Pathogens》上的一篇研究報告中，來(lái)自加拿大麥克馬斯特大學(xué)的研究者表示，我們機體的免疫系統并不會(huì )隨著(zhù)年齡的增長(cháng)而關(guān)閉。這項研究揭示了一組特殊類(lèi)別的免疫細胞，名為T(mén)細胞，在老年人機體中T細胞可以對病毒感染進(jìn)行反應，而且T細胞的反應能力及活性與來(lái)自年輕人體內的T細胞活力一樣。

　　研究者Jonathan Bramson表示，長(cháng)期以來(lái)，人們一直認為老年人感染病毒細菌的風(fēng)險較高，因為老年人缺少免疫細胞，但是實(shí)際上并不是這樣，這樣研究中，研究者研究發(fā)現，老年人依然有足夠的免疫力來(lái)抵御病毒的感染。

　　文章中，研究者對年齡小于40的個(gè)體、41至59歲以及超過(guò)60歲的，感染三種不同病毒（包括西尼羅病毒）的個(gè)體進(jìn)行研究，發(fā)現老年人一組同樣也表現出了正常的免疫系統反應。抵御病毒的T細胞數量以及功能性的T細胞數量在三個(gè)研究群體中都是等同的。

　　研究者Bramson說(shuō)，因此隨著(zhù)我們年齡增長(cháng)，我們機體仍然可以對病毒產(chǎn)生較強的免疫反應，而且這種免疫反應能力與年輕時(shí)候是一樣的。

　　本文的研究結果對于開(kāi)發(fā)老年人專(zhuān)用的疫苗具有重要的指示意義。當然，針對于老年人的疫苗很難開(kāi)發(fā)出來(lái)以引起機體免疫細胞的反應，這項研究或幫助解釋流感疫苗有效保護效應的缺失。本文研究揭示了，疫苗可以被特異性地開(kāi)發(fā)出來(lái)來(lái)產(chǎn)生T細胞免疫力，這或許可以更加有效地保護老年人。

　　這項研究由加拿大衛生研究院以及美國**衛生院提供資助。
 

　　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.