期刊
CELL CALCIUM
卷 90, 期 -, 页码 -出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2020.102227
关键词
B cells; CRAC; STIM1; STIM2; Apoptosis; mTORC1; NFAT; NF-kappaB; Calcium
类别
资金
- NIH [AI097302, AI130143, AI137004]
- Irma T. Hirschl career scientist award
B lymphocytes are an important component of the adaptive and innate immune system because of their ability to secrete antibodies and to present antigens to T cells, which is critical for immune responses to many pathogens. Abnormal B cell function is the cause of diseases including autoimmune, paraneoplastic, and immunodeficiency disorders. The development, survival, and function of B cells depend on signaling through the B cell receptor (BCR) and costimulatory receptors. One of the signaling pathways induced by antigen binding to the BCR is store-operated Ca2+ entry (SOCE), which depends on the Ca2+ channel ORAI1 and its activators stromal interaction molecule (STIM) 1 and 2. A recent study by Berry a al. [1] reports that B cells lacking STIM1 and STIM2 fail to survive and proliferate because abolished SOCE results in impaired expression of two key antiapoptotic genes and blunted activation of mTORC1 and c-Myc signaling. The associated Ca2+ regulated checkpoints of B cell survival and proliferation can be bypassed, at least partially, by costimulation through CD40 or TLR9. This study provides important new insights on how SOCE controls B cell function.
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