期刊
IMMUNITY
卷 44, 期 4, 页码 782-794出版社
CELL PRESS
DOI: 10.1016/j.immuni.2016.01.015
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-
类别
资金
- NIH [5T32HL789315, HL097111, 5R01NS081916, 5R37GM53950, 1R01AI095308]
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 Ca(V)3.1 calcium channel. Ca(V)3.1 mediated a substantial current at resting membrane potentials, and its deficiency had no effect on TCR-initiated calcium entry. Mice deficient for Ca(V)3.1 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. Ca(V)3.1 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 Ca(V)3.1-deficient T cells. These data provide evidence for T-type channels in immune cells and their potential role in shaping the autoimmune response.
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