TY - JOUR
T1 - The role of K+ in the regulation of the increase in intracellular Ca2+ mediated by the T lymphocyte antigen receptor
AU - Gray, Lloyd S.
AU - Gnarra, James R.
AU - Russell, John H.
AU - Engelhard, Victor H.
N1 - Funding Information:
We would like to thank Mrs. Pam Shumaker for preparation of the manuscript. We are grateful for the critical comments of Drs. D. Cafiso and H. Kutchai. This work is supported in part by U. S. Public Health Service Grants Al 20983, Al 21393, CA 28533, and RR 05431. V. H. E. is the recipient of Research Career Development Award CA 00835, and J. H. R. is the recipient of Research Career Development Award CA 00926.
PY - 1987/7/3
Y1 - 1987/7/3
N2 - 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.
AB - 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.
UR - https://www.scopus.com/pages/publications/0023636265
U2 - 10.1016/0092-8674(87)90668-4
DO - 10.1016/0092-8674(87)90668-4
M3 - Article
C2 - 2439211
AN - SCOPUS:0023636265
SN - 0092-8674
VL - 50
SP - 119
EP - 127
JO - Cell
JF - Cell
IS - 1
ER -