据美国每日科学网站报道，英国研究人员发现了一种可控制白血细胞老化的新机制，可扭转免疫系统衰退，提高老年人的免疫力。该研究发表在《免疫学期刊》上。
随着年龄的增长，老年人免疫系统的效率开始下降，因而容易感染重症。这对他们的生活健康构成了威胁，也使其生活质量明显下降。
由伦敦大学学院阿恩·阿克巴尔教授领导的研究小组发现，人类免疫系统逐渐衰弱的原因是由于每次感染后会有一定比例的白血细胞失活。虽然这种机制是进化而来，可以起到预防某些癌症的作用，但随着失活的白血细胞的比例不断提高，人体的防御系统也被削弱。
研究表明，白血细胞失活是由一种尚不确定的免疫系统老化机制所导致。此前科学家认为，免疫细胞老化与染色体端粒的长度有关。随着白血细胞的不断增殖，染色体端粒不断缩短，直至最后细胞永久失活。这意味着，免疫细胞有一种内置的寿命机制。随着人类寿命的延长，免疫细胞将无法提供有效的保护。
阿克巴尔教授的研究小组在采集的血液样本中发现，一些失活的白血细胞却有着较长的端粒，这表明白血细胞失活存在其他机制。而更令人兴奋的是，这些有着较长端粒的白血细胞不会处于永久失活状态。
当研究人员阻断在实验室中新确定的白血细胞的某个途径时发现，白血细胞可以被重新激活，而阻断该途径的药物早已被开发出来，用于治疗其他疾病。所以研究人员下一步将研究重新激活老年人的白血细胞会带来什么好处。
研究人员表示，虽然这种方法还不能让人类永葆青春，但它可以提高老年人的免疫力，帮助老年人战胜各种感染性疾病。此外，该研究还深化了人类对细胞生物学的认识，为控制人类的免疫系统开拓出全新的无法预见的未来，对提高人类的生活质量价值重大。(生物谷 Bioon.com)
doi:10.4049/?jimmunol.1100978
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Reversible Senescence in Human CD4+CD45RA+CD27− Memory T Cells
Diletta Di Mitri, Rita I. Azevedo, Sian M. Henson, Valentina Libri, Natalie E. Riddell, Richard Macaulay, David Kipling, Maria V. D. Soares, Luca Battistini and Arne N. Akbar
Persistent viral infections and inflammatory syndromes induce the accumulation of T cells with characteristics of terminal differentiation or senescence. However, the mechanism that regulates the end-stage differentiation of these cells is unclear. Human CD4+ effector memory (EM) T cells (CD27−CD45RA−) and also EM T cells that re-express CD45RA (CD27−CD45RA+; EMRA) have many characteristics of end-stage differentiation. These include the expression of surface KLRG1 and CD57, reduced replicative capacity, decreased survival, and high expression of nuclear γH2AX after TCR activation. A paradoxical observation was that although CD4+ EMRA T cells exhibit defective telomerase activity after activation, they have significantly longer telomeres than central memory (CM)-like (CD27+CD45RA−) and EM (CD27−CD45RA−) CD4+ T cells. This suggested that telomerase activity was actively inhibited in this population. Because proinflammatory cytokines such as TNF-α inhibited telomerase activity in T cells via a p38 MAPK pathway, we investigated the involvement of p38 signaling in CD4+ EMRA T cells. We found that the expression of both total and phosphorylated p38 was highest in the EM and EMRA compared with that of other CD4+ T cell subsets. Furthermore, the inhibition of p38 signaling, especially in CD4+ EMRA T cells, significantly enhanced their telomerase activity and survival after TCR activation. Thus, activation of the p38 MAPK pathway is directly involved in certain senescence characteristics of highly differentiated CD4+ T cells. In particular, CD4+ EMRA T cells have features of telomere-independent senescence that are regulated by active cell signaling pathways that are reversible.