作者: E Donnadieu , G Bismuth , A Trautmann
DOI: 10.1016/S0021-9258(18)35689-8
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摘要: Mechanisms controlling Ca2+ fluxes through the plasma membrane of lymphocytes have been characterized in a human T-cell clone and Jurkat line. Due to endogenous buffers, about 1/125 ions that enter cell are free. were estimated from variations intracellular concentration ([Ca2+]i) elicited by jumps extracellular ([Ca2+]o). Thapsigargin was used inhibit uptake into stores stimulate entry. extrusion strictly due activity Ca(2+)-ATPases since there no detectable Na+/Ca2+ exchange these cells. The rate mainly influenced [Ca2+]i less [Ca2+]o but insensitive depolarization. In depolarized cells, thapsigargin-induced influx reduced 10% value measured normally polarized suggesting depolarization not only reduces electrochemical gradient for ions, also inhibits permeation. When cell, they bind site inside channel, with Kd 3.3 mM. Stimulation clonal T-cells low concentrations either anti-CD3 antibodies or thapsigargin oscillations. Both amplitude frequency CD3-induced oscillations sensitive [Ca2+]o. These immediately interrupted when removed. properties T suggest influx, modulated [Ca2+]i.