CELL CYCLE AND APOPTOSIS GENES IN IMMUNOLOGIC SENESCENCE

描述（改编自研究者摘要）：本申请是 基于T细胞的免疫衰老是 这是两个同时发生的相互关联的事件的结果。 T细胞库是 由一个扩大的记忆淋巴细胞库重塑。 记忆T细胞 他们自己达到一个难治性（无反应性）状态，表现为进一步 对进一步活化、细胞周期进入和凋亡的抗性。 第一 效应归因于初始细胞被累积的细胞因子稀释。 记忆表型细胞，导致整体剧目收缩。 的 第二个效应归因于一个世代时钟， 分配的激活和细胞分裂的记忆T细胞之前的数量 主要通过细胞周期蛋白激酶的积累促进复制性衰老 抑制剂的 这些对衰老T细胞的细胞周期和凋亡的研究， 有助于定义与以下相关的分子缺陷： 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.