| First Author | Matsumoto M | Year | 2011 |
| Journal | Immunity | Volume | 34 |
| Issue | 5 | Pages | 703-14 |
| PubMed ID | 21530328 | Mgi Jnum | J:172608 |
| Mgi Id | MGI:5008356 | Doi | 10.1016/j.immuni.2011.03.016 |
| Citation | Matsumoto M, et al. (2011) The Calcium Sensors STIM1 and STIM2 Control B Cell Regulatory Function through Interleukin-10 Production. Immunity 34(5):703-14 |
| abstractText | A chief Ca(2+) entry pathway in immune cells is store-operated Ca(2+) (SOC) influx, which is triggered by depletion of Ca(2+) from the endoplasmic reticulum (ER). However, its physiological role in B cells remains elusive. Here, we show that ER calcium sensors STIM1- and STIM2-induced SOC influx is critical for B cell regulatory function. B cell-specific deletion of STIM1 and STIM2 in mice caused a profound defect in B cell receptor (BCR)-induced SOC influx and proliferation. However, B cell development and antibody responses were unaffected. Remarkably, B cells lacking both STIM proteins failed to produce the anti-inflammatory cytokine IL-10 because of defective activation of nuclear factor of activated T cells (NFAT) after BCR stimulation. This resulted in exacerbation of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. Our data establish STIM-dependent SOC influx as a key signal for B cell regulatory function required to limit autoimmunity. |
