Low-Voltage-Activated CaV3.1 Calcium Channels Shape T Helper Cell Cytokine Profiles

Huiyun Wang, Xuexin Zhang, Li Xue, Juan Xing, Marie Hélène Jouvin, James W. Putney, Matthew P. Anderson, Mohamed Trebak, Jean Pierre Kinet

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

Activation of T cells is mediated by the engagement of T cell receptors (TCRs) followed by calcium entry via store-operated calcium channels. Here we have shown an additional route for calcium entry into T cells-through the low-voltage-activated T-type CaV3.1 calcium channel. CaV3.1 mediated a substantial current at resting membrane potentials, and its deficiency had no effect on TCR-initiated calcium entry. Mice deficient for CaV3.1 were resistant to the induction of experimental autoimmune encephalomyelitis and had reduced productions of the granulocyte-macrophage colony-stimulating factor (GM-CSF) by central nervous system (CNS)-infiltrating T helper 1 (Th1) and Th17 cells. CaV3.1 deficiency led to decreased secretion of GM-CSF from in vitro polarized Th1 and Th17 cells. Nuclear translocation of the nuclear factor of activated T cell (NFAT) was also reduced in CaV3.1-deficient T cells. These data provide evidence for T-type channels in immune cells and their potential role in shaping the autoimmune response.

Original languageEnglish (US)
Pages (from-to)782-794
Number of pages13
JournalImmunity
Volume44
Issue number4
DOIs
StatePublished - Apr 19 2016

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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