近日，刊登在國際著名雜志《PLoS Pathogens》上的一篇研究報告中，來自加拿大麥克馬斯特大學(xué)的研究者表示，我們機(jī)體的免疫系統(tǒng)并不會隨著年齡的增長而關(guān)閉。這項(xiàng)研究揭示了一組特殊類別的免疫細(xì)胞，名為T細(xì)胞，在老年人機(jī)體中T細(xì)胞可以對病毒感染進(jìn)行反應(yīng)，而且T細(xì)胞的反應(yīng)能力及活性與來自年輕人體內(nèi)的T細(xì)胞活力一樣。

　　研究者Jonathan Bramson表示，長期以來，人們一直認(rèn)為老年人感染病毒細(xì)菌的風(fēng)險較高，因?yàn)槔夏耆巳鄙倜庖呒?xì)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(xiàn)，老年人依然有足夠的免疫力來抵御病毒的感染。

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

　　研究者Bramson說，因此隨著我們年齡增長，我們機(jī)體仍然可以對病毒產(chǎn)生較強(qiáng)的免疫反應(yīng)，而且這種免疫反應(yīng)能力與年輕時候是一樣的。

　　本文的研究結(jié)果對于開發(fā)老年人專用的疫苗具有重要的指示意義。當(dāng)然，針對于老年人的疫苗很難開發(fā)出來以引起機(jī)體免疫細(xì)胞的反應(yīng)，這項(xiàng)研究或幫助解釋流感疫苗有效保護(hù)效應(yīng)的缺失。本文研究揭示了，疫苗可以被特異性地開發(fā)出來來產(chǎn)生T細(xì)胞免疫力，這或許可以更加有效地保護(hù)老年人。

　　這項(xiàng)研究由加拿大衛(wèi)生研究院以及美國**衛(wèi)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.