INTRACELLULAR CA2+ REGULATION IN CD3 STIMULATED JURKAT T-CELLS INVOLVES H+ FLUXES
INTRACELLULAR CA2+ REGULATION IN CD3 STIMULATED JURKAT T-CELLS INVOLVES H+ FLUXES
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DOI：
10.1016/0898-6568(91)90075-6
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发表时间：
1991-01-01
影响因子：
4.8
通讯作者：
BREITTMAYER, JP
中科院分区：
文献类型：
--
作者：
BERTHE, P;COUSIN, JL;BREITTMAYER, JP
触发T淋巴细胞的CD3/TCR复合体诱导胞质游离钙快速上升，随后缓慢下降。这个平台的水平取决于外部pH值，碱化介质越多，pH值就越高。无论是单抗的pH依赖性结合，还是内部pH的扰动都不能解释这种效应。在无钠的培养基中，或在二甲氨酰Ca2+的存在下，升高伴随着细胞的酸化；它们都在同样程度上依赖于外部钙浓度。TPA抑制CD3-，但不抑制离子霉素诱导的Ca2+和H+升高，表明它更可能作用于Ca2+内流，而不是其外排。这些结果表明，细胞内钙可能受到Ca2+/H+ atp酶的调节，该酶驱动H+进入和Ca2+排出。在外部Na+存在的情况下，H+应通过Na+/H+交换器返回介质。
Triggering the CD3/TCR complex of T lymphocytes induces a rapid rise in cytosolic free calcium followed by a slowly declining plateau. The level of this plateau depends on external pH, the more alkalinized media leading to higher values. Neither a pH-dependent binding of mAb, nor a perturbation of internal pH can account for this effect. In a sodium-free medium, or in the presence of dimethylamiloride Ca2+, elevation is accompanied by an acidification of the cells; both of them depend, to the same extent, on external calcium concentration. TPA inhibits CD3-, but not ionomycin-induced Ca2+ and H+ raises, indicating that it acts more probably on Ca2+ influx, rather than on its efflux. These results suggest that intracellular calcium could be regulated by a Ca2+/H+ ATPase which drives H+ in and Ca2+ out. In the presence of external Na+, H+ should return to the medium by the Na+/H+ exchanger.