Journal
NATURE IMMUNOLOGY
Volume 9, Issue 4, Pages 432-443Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1574
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Funding
- NIAID NIH HHS [R01 AI040127-17, R01 AI048213-08, R01 AI040127, R01 AI048213] Funding Source: Medline
- NIGMS NIH HHS [R01 GM075256-03, R01 GM075256] Funding Source: Medline
- NINDS NIH HHS [R01 NS057499, R01 NS057499-02, R01 NS057499-01] Funding Source: Medline
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Store-operated Ca2+ entry through calcium release-activated calcium channels is the chief mechanism for increasing intracellular Ca2+ in immune cells. Here we show that mouse T cells and fibroblasts lacking the calcium sensor STIM1 had severely impaired store-operated Ca2+ influx, whereas deficiency in the calcium sensor STIM2 had a smaller effect. However, T cells lacking either STIM1 or STIM2 had much less cytokine production and nuclear translocation of the transcription factor NFAT. T cell-specific ablation of both STIM1 and STIM2 resulted in a notable lymphoproliferative phenotype and a selective decrease in regulatory T cell numbers. We conclude that both STIM1 and STIM2 promote store-operated Ca2+ entry into T cells and fibroblasts and that STIM proteins are required for the development and function of regulatory T cells.
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