CELL CYCLE AND APOPTOSIS GENES IN IMMUNOLOGIC SENESCENCE

描述(改编自调查者摘要)：此应用程序是 基于T细胞的免疫衰老是 两个同时发生且相互关联的事件的结果。T细胞的谱系是 由扩大的记忆淋巴细胞池重塑。记忆T细胞 自身达到一种难解(无能)状态，表现为进一步 抵抗进一步的激活、细胞周期进入和细胞凋亡。第一 这种作用归因于对幼稚细胞的稀释 记忆表型细胞，导致总的谱系收缩。这个 第二个效应归因于一种记录了 记忆T细胞之前分配的激活数和细胞分裂数 主要通过细胞周期蛋白激酶的积聚促进复制性衰老 抑制剂。这些关于衰老T细胞的细胞周期和凋亡的研究将 有助于定义与之相关的分子缺陷 免疫衰老。

DESCRIPTION (Adapted from the Investigator's abstract): This application is based on the hypothesis that immunologic senescence of T-cells is the results of two concurrent and interrelated events. The T-cell repertoire is reshaped by an expanded memory lymphocyte pool. The memory T-cells themselves reach a refractory (anergic) state manifested by further resistance to further activation, cell cycle entry and apoptosis. The first effect is attributed to the dilution of naive cells by the accumulated memory phenotype cells that leads to overall repertoire constrictions. The second effect is attributed to a generational clock that records an allocated number of activations and cell divisions by memory T-cells before promoting replicative senescence primarily by the buildup of cyclin kinase inhibitors. These studies of cell cycle and apoptosis of aged T-cells will be instrumental to defining the molecular defects associated with immunologic senescence.