Thoman M L
Department of Immunology, Research Institute of Scripps Clinic, La Jolla, California 92037.
Cell Immunol. 1991 Jul;135(2):410-7. doi: 10.1016/0008-8749(91)90286-k.
IL-2 receptor-bearing splenic T lymphocytes derived from aged C57BL6/J mice (22-24 months) display a relative inability to respond to IL-2 when compared to similar cells from young (2-3 months) animals. As a population the aged cells incorporate less [3H]thymidine and fewer are able to undergo vigorous clonal growth. Both the CD4+ and CD8+ subsets display these defects. The clonal assay indicates that aged T cells, in addition to having longer cell cycle transit time, also have a higher frequency of cell cycle arrest than similarly activated young T cells. This defect in IL-2 responsiveness is distinct from those in early signal transduction which limit aged T lymphocyte entry into cycle and cannot be corrected by phorbol myristate acetate or ionomycin.
与年轻（2 - 3个月）动物的类似细胞相比，源自老龄C57BL6/J小鼠（22 - 24个月）的携带白细胞介素-2（IL-2）受体的脾T淋巴细胞对IL-2的反应相对较弱。作为一个群体，老龄细胞掺入的[3H]胸腺嘧啶核苷较少，能够进行旺盛克隆生长的细胞也较少。CD4+和CD8+亚群均表现出这些缺陷。克隆试验表明，老龄T细胞除了细胞周期转运时间较长外，与同样被激活的年轻T细胞相比，细胞周期停滞的频率也更高。IL-2反应性的这种缺陷与早期信号转导中的缺陷不同，早期信号转导缺陷限制老龄T淋巴细胞进入细胞周期，且不能被佛波醇肉豆蔻酸酯乙酸盐或离子霉素纠正。
