科学家发现控制人体白细胞老化的分子机制（图）
英国科学家们发现了一种新的分子机制可以控制白细胞的活力。该研究的论文发表在最新一期的《Journal of Immunology》杂志上，这项发现将有助于人们开发逆转人体免疫系统老化的方法，以便在未来在临床上可以短期的增强老年人的免疫力。
免疫力下降对于老年人来说是一个非常严重的问题，它会导致人体容易受外界各种病毒和细菌的感染等等，进而影响人体健康和生活质量。
论文的通讯作者，伦敦大学学院的Arne Akbar教授说道：“人体的免疫系统会随着时间的流逝而逐渐弱化，因为我们的身体每抵御一次外界的感染，都会使部分的白细胞中的DNA端粒在细胞复制过程中逐渐丢失，随着端粒的变短，这些细胞也失去活力，并且这也是几种癌症发生的主要原因。”
Arne Akbar教授继续说道：“我们的这项研究发现了使这些免疫系统中的白细胞失去活力的分子机制，这在以前从未被报道过。但是我们不想将这些细胞永久性的激活，而是让其在短期内处于激活状态。”
Akbar的研究小组在研究一些血液样本时发现有些白细胞在端粒仍然很长但失去了活力。这提示人体免疫系统还存在其它机制诱导白细胞失活，并且科学家们还认为通过适当的方法能让这些失活的白细胞恢复活力。
科学家们在实验室中通过阻断名为p38 MAPK的信号通路能使得白细胞被重新激活。相关的阻断信号药物也已经在研发过程中，研究人员打算将其用于老年人身上，以观察其对于人体免疫系统是否有益。
生物科学与生物技术协会会长Douglas Kell教授说道：“该研究发现了调控我们人体免疫系统的新机制，进一步加深我们对细胞功能机制的理解。同时，未来我们可以研发相关的药物用于帮助那些老年人增强人体免疫力，以便有效抵抗疾病，恢复他们的健康并提高生活质量。”（生物探索 Jun译）
生物探索推荐英文论文原文摘要：
Reversible Senescence in Human CD4+CD45RA+CD27− Memory T Cells
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.
