钾离子在调节由T淋巴细胞抗原受体介导的细胞内钙离子增加中的作用。

The role of K+ in the regulation of the increase in intracellular Ca2+ mediated by the T lymphocyte antigen receptor.

作者信息

Gray L S, Gnarra J R, Russell J H, Engelhard V H

出版信息

Cell. 1987 Jul 3;50(1):119-27. doi: 10.1016/0092-8674(87)90668-4.

Abstract

The regulation of the increase in intracellular calcium ([Ca2+]i) occurring in cytolytic T lymphocytes (CTLs) upon their interaction with antigen was examined. This [Ca2+]i increase and lytic function were insensitive to verapamil, a Ca channel blocker. An antigen-independent increase in [Ca2+]i was not induced by depolarization of CTLs with excess extracellular K+, suggesting that Ca2+ influx is not mediated by the ubiquitous voltage-gated Ca channel. The antigen-induced [Ca2+]i increase was inhibited by prior membrane hyperpolarization with valinomycin. Hyperpolarization occurred under normal circumstances in CTLs exposed to antigen-receptor-specific antibodies. This potential change was Ca2+-dependent and inhibited by K channel blockade. Conversely, K channel blockade augmented the antigen-specific [Ca2+]i increase while markedly decreasing the K+ efflux associated with CTL lytic function. Therefore, either membrane potential or intracellular K+ regulates the antigen-specific [Ca2+]i increase in CTLs.

摘要

研究了细胞毒性T淋巴细胞（CTL）与抗原相互作用时细胞内钙浓度（[Ca2+]i）升高的调节机制。这种[Ca2+]i升高和裂解功能对钙通道阻滞剂维拉帕米不敏感。用过量细胞外K+使CTL去极化并不能诱导[Ca2+]i的非抗原依赖性升高，这表明Ca2+内流不是由普遍存在的电压门控钙通道介导的。用缬氨霉素预先使细胞膜超极化可抑制抗原诱导的[Ca2+]i升高。在正常情况下，暴露于抗原受体特异性抗体的CTL会发生超极化。这种电位变化依赖于Ca2+，并可被钾通道阻断所抑制。相反，钾通道阻断增强了抗原特异性的[Ca2+]i升高，同时显著降低了与CTL裂解功能相关的K+外流。因此，膜电位或细胞内K+调节CTL中抗原特异性的[Ca2+]i升高。