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激活驱动的程序性细胞死亡与T细胞受体ζη表达

Activation-driven programmed cell death and T cell receptor zeta eta expression.

作者信息

Merćep M, Weissman A M, Frank S J, Klausner R D, Ashwell J D

机构信息

Biological Response Modifiers Program, National Cancer Institute, Bethesda, MD 20892.

出版信息

Science. 1989 Dec 1;246(4934):1162-5. doi: 10.1126/science.2531464.

Abstract

Activation of spontaneously dividing T cell hybridomas induces interleukin-2 (IL-2) production, a cell cycle block, and programmed cell death. T cell hybridomas that express the T cell antigen receptor (TCR) zeta homodimer (zeta 2), but not the TCR zeta eta heterodimer, were studied. The zeta eta- cells produced little or no inositol phosphates (IP) when stimulated with antigen. In most cases the hydrolysis of phosphoinositides was also impaired after stimulation with antibody to CD3, although one zeta eta- cell produced normal concentrations of IP. The zeta eta- cells slowed their growth and secreted IL-2 in response to both stimuli. However, the zeta eta- cells did not die after activation with antigen. Since activated thymocytes also undergo programmed cell death, these results may have important implications for the role of the zeta eta.TCR in negative selection.

摘要

自发分裂的T细胞杂交瘤的激活可诱导白细胞介素-2(IL-2)的产生、细胞周期阻滞和程序性细胞死亡。对表达T细胞抗原受体(TCR)ζ同型二聚体(ζ2)而非TCR ζη异型二聚体的T细胞杂交瘤进行了研究。ζη-细胞在用抗原刺激时产生很少或不产生肌醇磷酸(IP)。在大多数情况下,用抗CD3抗体刺激后,磷酸肌醇的水解也受到损害,尽管一个ζη-细胞产生正常浓度的IP。ζη-细胞对两种刺激均反应为生长减慢并分泌IL-2。然而,ζη-细胞在用抗原激活后并未死亡。由于活化的胸腺细胞也会经历程序性细胞死亡,这些结果可能对ζη.TCR在阴性选择中的作用具有重要意义。

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