Distinct Mechanisms for Ca2+ Entry Induced by OKT3 and Ca2+ Depletion in Jurkat T Cells

Ca2+ influx triggered by antigen binding to T cell receptors (TCR) is an early event in T cell activation. An additional (Ca2+ influx induced by depletion of intracellular Ca2+ (CDCI) has been characterized in human Jurkat T cells that is both temporally and mechanistically distinct from TCR-mediate...

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Bibliographic Details
Published in:Experimental cell research 1995-01, Vol.216 (1), p.222-231
Main Authors: Sei, Yoshitatsu, Takemura, Motohiko, Gusovsky, Fabian, Skolnick, Phil, Basile, Anthony
Format: Article
Language:English
Subjects:
8-Bromo Cyclic Adenosine Monophosphate - pharmacology
Bucladesine - pharmacology
Calcium - metabolism
Calcium Channel Blockers - pharmacology
Cations, Divalent - metabolism
Cholera Toxin - pharmacology
Colforsin - analogs & derivatives
Colforsin - pharmacology
Humans
Inositol Phosphates - biosynthesis
Ion Channel Gating - drug effects
Ion Channel Gating - physiology
Ion Transport
Lymphocyte Activation - physiology
Muromonab-CD3
Pertussis Toxin
Receptors, Antigen, T-Cell - metabolism
T-Lymphocytes - metabolism
Tetradecanoylphorbol Acetate - pharmacology
Tumor Cells, Cultured
Virulence Factors, Bordetella - pharmacology
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Summary:Ca2+ influx triggered by antigen binding to T cell receptors (TCR) is an early event in T cell activation. An additional (Ca2+ influx induced by depletion of intracellular Ca2+ (CDCI) has been characterized in human Jurkat T cells that is both temporally and mechanistically distinct from TCR-mediated Ca2+ influx (TCRCI). Both TCRCI and CDCI were insensitive to voltage-gated Ca2+ channel antagonists (e.g., nifedipine, verapamil, and ω-conotoxin G) and pertussis toxin, yet were voltage-sensitive and inhibited by SKF 96365 (a receptorgated Ca2+ channel blocker) and cholera toxin. However, TCRCI but not CDCI was associated with a significant increase in inositol phosphate (IPx) levels and inhibited by phorbol ester, while CDCI but not TCRCI was inhibited by Sr2+, forskolin (FSK), and 1,9-dideoxy FSK in a cAMP-independent fashion. Moreover, TCR stimulation did not deplete thapsigargin-sensitive Ca2+ stores, suggesting that TCRCI is not merely a consequence of Ca2+ depletion. These results indicate that Ca2+ entry following the depletion of intracellular Ca2+ stores or TCR stimulation occur through distinct cellular mechanisms coexisting in Jurkat T cells.
ISSN:0014-4827
1090-2422
DOI:10.1006/excr.1995.1028