The JI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     
 

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kerschbaum, H. H.
Right arrow Articles by Cahalan, M. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kerschbaum, H. H.
Right arrow Articles by Cahalan, M. D.

The Journal of Immunology, Vol 159, Issue 4 1628-1638, Copyright © 1997 by American Association of Immunologists

ARTICLES

Ion channels, Ca2+ signaling, and reporter gene expression in antigen- specific mouse T cells

HH Kerschbaum, PA Negulescu and MD Cahalan
Department of Physiology and Biophysics, University of California, Irvine 92717, USA.

Whole cell recordings were performed in parallel with measurements of intracellular Ca2+ ([Ca2+]i) and gene expression using the murine T cell hybridoma, B3Z, a cell line stably infected with a lacZ reporter gene, driven by the minimal IL-2 promoter (NF-AT, nuclear factor of activated T cells). The physiologic roles of ion channels in B3Z cells were investigated by correlating the pharmacology of channel block with [Ca2+]i, and expression of lacZ. In B3Z cells and activated human T cells, the major component of voltage-gated K+ (K(V)) current had biophysical and pharmacologic properties associated with type n channels encoded by Kv1.3; a minor K(V) component was charybdotoxin (CTX) resistant. Ca2+-activated K+ (K(Ca)) current was sensitive to CTX, but not to margatoxin (MgTX). Inwardly rectifying K+ (K(IR)) current was blocked completely by 200 microM of Ba2+. Outwardly rectifying Cl- currents were induced by cell swelling. An inwardly rectifying Ca2+ current (I(CRAC)) was activated by dialyzing the cell with 10 mM EGTA and 10 microM IP3. CTX reduced thapsigargin-stimulated [Ca2+]i signaling and gene expression by approximately 25%. Although the thapsigargin-stimulated [Ca2+]i signal was resistant to complete inhibition by K+ channel blockers, it was very sensitive to the K+ diffusion potential and Cl- removal, suggesting that drug-resistant K+ channels and perhaps Cl- channels can maintain a sufficiently negative membrane potential to drive Ca2+ influx. Neither [Ca2+]i signaling nor gene expression induced by stimulation of the CD3-epsilon subunit of the TCR was inhibited by ion channel blockers used in this study. We conclude that several channel types can contribute to maintenance of Vm, Ca2+ signals, and gene expression.


This article has been cited by other articles:


Home page
 J. Pharmacol. Exp. Ther.Home page
B. S. Fischer, D. Qin, K. Kim, and T. V. McDonald
Capsaicin Inhibits Jurkat T-Cell Activation by Blocking Calcium Entry Current ICRAC
J. Pharmacol. Exp. Ther., October 1, 2001; 299(1): 238 - 246.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
B. Nilius and G. Droogmans
Ion Channels and Their Functional Role in Vascular Endothelium
Physiol Rev, October 1, 2001; 81(4): 1415 - 1459.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
C. Beeton, J. Barbaria, P. Giraud, J. Devaux, A.-M. Benoliel, M. Gola, J. M. Sabatier, D. Bernard, M. Crest, and E. Beraud
Selective Blocking of Voltage-Gated K+ Channels Improves Experimental Autoimmune Encephalomyelitis and Inhibits T Cell Activation
J. Immunol., January 15, 2001; 166(2): 936 - 944.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
F. D. Goldman, A. L. Gilman, C. Hollenback, R. M. Kato, B. A. Premack, and D. J. Rawlings
Hydroxychloroquine inhibits calcium signals in T cells: a new mechanism to explain its immunomodulatory properties
Blood, June 1, 2000; 95(11): 3460 - 3466.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
C. M. Fanger, A. L. Neben, and M. D. Cahalan
Differential Ca2+ Influx, KCa Channel Activity, and Ca2+ Clearance Distinguish Th1 and Th2 Lymphocytes
J. Immunol., February 1, 2000; 164(3): 1153 - 1160.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
A. D. Gruber and B. U. Pauli
Tumorigenicity of Human Breast Cancer Is Associated with Loss of the Ca2+-activated Chloride Channel CLCA2
Cancer Res., November 1, 1999; 59(21): 5488 - 5491.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
X. Wei, B. J. Tromberg, and M. D. Cahalan
Mapping the sensitivity of T cells with an optical trap: Polarity and minimal number of receptors for Ca2+ signaling
PNAS, July 20, 1999; 96(15): 8471 - 8476.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
L. M. Schwiebert, K. Estell, and S. M. Propst
Chemokine expression in CF epithelia: implications for the role of CFTR in RANTES expression
Am J Physiol Cell Physiol, March 1, 1999; 276(3): C700 - C710.
[Abstract] [Full Text] [PDF]

Home page
 J. Exp. Med.Home page
G. R. Ehring, H. H. Kerschbaum, C. Eder, A. L. Neben, C. M. Fanger, R. M. Khoury, P. A. Negulescu, and M. D. Cahalan
A Nongenomic Mechanism for Progesterone-mediated Immunosuppression: Inhibition of K+ Channels, Ca2+ Signaling, and Gene Expression in T Lymphocytes
J. Exp. Med., November 2, 1998; 188(9): 1593 - 1602.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1997 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1997 by The American Association of Immunologists, Inc. All rights reserved.