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What’s Bred in the Bone: Calcium Channels in Lymphocytes

Franz Fenninger and Wilfred A. Jefferies
J Immunol February 15, 2019, 202 (4) 1021-1030; DOI: https://doi.org/10.4049/jimmunol.1800837
Franz Fenninger
Michael Smith Laboratories, University of British Columbia, Vancouver V6T 1Z4, British Columbia, Canada;Department of Microbiology and Immunology, University of British Columbia, Vancouver V6T 1Z3, British Columbia, Canada;
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Wilfred A. Jefferies
Michael Smith Laboratories, University of British Columbia, Vancouver V6T 1Z4, British Columbia, Canada;Department of Microbiology and Immunology, University of British Columbia, Vancouver V6T 1Z3, British Columbia, Canada;Vancouver Prostate Centre, University of British Columbia, Vancouver V6H 3Z6, British Columbia, Canada;Centre for Blood Research, University of British Columbia, Vancouver V6T 1Z4, British Columbia, Canada;The Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver V6T 1Z3, British Columbia, Canada;Department of Medical Genetics, University of British Columbia, Vancouver V6T 1Z4, British Columbia, Canada; andDepartment of Zoology, University of British Columbia, Vancouver V6T 1Z4, British Columbia, Canada
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Abstract

Calcium (Ca2+) is an important second messenger in lymphocytes and is essential in regulating various intracellular pathways that control critical cell functions. Ca2+ channels are located in the plasma membrane and intracellular membranes, facilitating Ca2+ entry into the cytoplasm. Upon Ag receptor stimulation, Ca2+ can enter the lymphocyte via the Ca2+ release-activated Ca2+ channel found in the plasma membrane. The increase of cytosolic Ca2+ modulates signaling pathways, resulting in the transcription of target genes implicated in differentiation, activation, proliferation, survival, and apoptosis of lymphocytes. Along with Ca2+ release-activated Ca2+ channels, several other channels have been found in the membranes of T and B lymphocytes contributing to key cellular events. Among them are the transient receptor potential channels, the P2X receptors, voltage-dependent Ca2+ channels, and the inositol 1,4,5-trisphosphate receptor as well as the N-methyl-d-aspartate receptors. In this article, we review the contributions of these channels to mediating Ca2+ currents that drive specific lymphocyte functions.

Footnotes

  • F.F. was supported by a DOC Fellowship of the Austrian Academy of Sciences. W.A.J. was supported by grants from the Canadian Institutes of Health Research (IPR-139079 and MOP-102698) and a grant from Pascal Biosciences, Inc.

  • Abbreviations used in this article:

    Ca2+
    calcium
    cADPR
    cyclic ADP-ribose
    CaV
    voltage-dependent Ca2+
    CFS/ME
    chronic fatigue syndrome/myalgic encephalomyelitis
    CRAC
    Ca2+ release-activated Ca2+
    EAE
    experimental autoimmune encephalomyelitis
    ER
    endoplasmic reticulum
    IP3
    inositol 1,4,5-trisphosphate
    KO
    knockout
    Na+
    sodium
    NMDA
    N-methyl-d-aspartate
    RyR
    ryanodine receptor
    SOCE
    store-operated Ca2+ entry
    STIM
    stromal interaction molecule
    TEff
    T effector
    Treg
    regulatory T cell
    TRP
    transient receptor potential.

  • Received June 14, 2018.
  • Accepted August 22, 2018.
  • Copyright © 2019 by The American Association of Immunologists, Inc.
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The Journal of Immunology: 202 (4)
The Journal of Immunology
Vol. 202, Issue 4
15 Feb 2019
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What’s Bred in the Bone: Calcium Channels in Lymphocytes
Franz Fenninger, Wilfred A. Jefferies
The Journal of Immunology February 15, 2019, 202 (4) 1021-1030; DOI: 10.4049/jimmunol.1800837

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What’s Bred in the Bone: Calcium Channels in Lymphocytes
Franz Fenninger, Wilfred A. Jefferies
The Journal of Immunology February 15, 2019, 202 (4) 1021-1030; DOI: 10.4049/jimmunol.1800837
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