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细胞毒性T淋巴细胞触发所需的蛋白激酶C。

Protein kinase C required for cytotoxic T lymphocyte triggering.

作者信息

Nishimura T, Burakoff S J, Herrmann S H

机构信息

Division of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA.

出版信息

J Immunol. 1987 Nov 1;139(9):2888-91.

PMID:3499460
Abstract

The role of protein kinase C (PK-C) in triggering the lytic response of cytotoxic T lymphocytes (CTL) has been examined. Both target cell lysis and the release of CTL-associated serine esterase (SE), a marker for cytotoxic granules, were used as indicators of the CTL lytic response. We found triggering of the CTL lytic response occurred when both a PK-C activator, phorbol 12-myristate 13-acetate (PMA), and a calcium ionophore, ionomycin, were added to CTL. The previously described inactivation of the CTL lytic response by long term treatment (24 hr) with PMA was also investigated. CTL cultured with PMA for 24 hr were unable to mediate target cell lysis or release SE; this inability to respond correlated with an absence of PK-C activity. Incubation of the PMA-treated CTL in the absence of PMA for an additional 24 hr resulted in recovery of PK-C activity, SE release, and the lytic response. These experiments strongly suggest that PK-C is involved with the transmembrane signaling required for SE release which is a necessary event in CTL-mediated target cell lysis.

摘要

蛋白激酶C(PK-C)在触发细胞毒性T淋巴细胞(CTL)的裂解反应中的作用已得到研究。靶细胞裂解以及细胞毒性颗粒标志物CTL相关丝氨酸酯酶(SE)的释放均被用作CTL裂解反应的指标。我们发现,当向CTL中同时添加PK-C激活剂佛波醇12-肉豆蔻酸酯13-乙酸酯(PMA)和钙离子载体离子霉素时,会触发CTL的裂解反应。我们还研究了先前描述的用PMA长期处理(24小时)导致CTL裂解反应失活的情况。用PMA培养24小时的CTL无法介导靶细胞裂解或释放SE;这种无反应能力与PK-C活性的缺失相关。在无PMA的情况下将经PMA处理的CTL再孵育24小时,会导致PK-C活性、SE释放和裂解反应的恢复。这些实验有力地表明,PK-C参与了SE释放所需的跨膜信号传导,而SE释放是CTL介导的靶细胞裂解中的一个必要事件。

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