Activation of mouse lymphocytes inhibits induction of rapid cell death by x-irradiation.
Activation of mouse lymphocytes inhibits induction of rapid cell death by x-irradiation.
复制标题
小鼠淋巴细胞的激活可抑制 X 射线照射引起的快速细胞死亡。
作者：
J. Lowenthal;A. W. Harris
静息淋巴细胞的一个显著特性是其在x射线照射后在间期迅速死亡的能力。BALB/c小鼠的胸腺细胞和外周淋巴细胞悬浮液用10至10，000拉德（0.1至100格雷）的剂量进行辐照，并通过伊红染料排除法在培养的3天内每隔一段时间测量其活力。在最初的几个小时的潜伏期后，活力以剂量依赖性方式呈指数下降。低至20拉德的剂量导致一些淋巴细胞迅速死亡。1000拉德照射后，90%的细胞在15~20小时内死亡，99%的细胞在25~35小时内死亡。外周淋巴细胞比胸腺细胞更早死亡，10，000拉德照射后死亡速度特别快。富集的T细胞和B细胞以相同的速率被辐射杀死，胸腺髓质细胞以与整个胸腺细胞群体相同的速率被杀死。与静止细胞相反，被有丝分裂原激活的T和B淋巴细胞不受如此快速的细胞死亡诱导。当不到1%的未受刺激淋巴细胞存活时，1000拉德的照射仅使活化细胞的活力降低了50%。类似地，抗原特异性辅助细胞和细胞毒性T细胞的克隆系在接受1000拉德后仅显示出延迟和缓慢的活力丧失。因此，激活状态可能是辐射免疫后果的重要决定因素。
A distinctive property of the resting lymphocyte is its ability to die rapidly in interphase after x-irradiation. Suspensions of thymocytes and peripheral lymphocytes from BALB/c mice were irradiated with doses ranging from 10 to 10,000 rad (0.1 to 100 Grays), and their viability was measured by eosin dye exclusion at intervals through 3 days of culture. After an initial latent period of a few hours, viability declined exponentially in a dose-dependent fashion. Doses as low as 20 rad caused some lymphocytes to die rapidly. After 1000 rad, 90% of the cells became nonviable in 15 to 20 hr and 99% in 25 to 35 hr. Peripheral lymphocytes showed a somewhat earlier loss of viability than did thymocytes, and were killed especially rapidly by 10,000 rad. Enriched T cells and B cells were killed by irradiation at equal rates, and medullary thymocytes were killed at the same rate as the whole thymocyte population. In contrast with resting cells, T and B lymphocytes activated by mitogens were not subject to such rapid induction of cell death. Irradiation with 1000 rad reduced the viability of activated cells by only 50% at a time when less than 1% of nonstimulated lymphocytes remained alive. Similarly, cloned lines of antigen-specific helper and cytotoxic T cells showed only a delayed and slow loss of viability after receiving 1000 rad. The state of activation can therefore be a significant determinant of the immunologic consequences of irradiation.