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 et 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 anti-apoptotic 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.

B 淋巴细胞是适应性和先天免疫系统的重要组成部分，因为它们能够分泌抗体并向 T 细胞呈递抗原，这对于对许多病原体的免疫反应至关重要。 B 细胞功能异常是导致自身免疫性疾病、副肿瘤性疾病和免疫缺陷性疾病等疾病的原因。 B 细胞的发育、存活和功能取决于 B 细胞受体 (BCR) 和共刺激受体的信号传导。抗原与 BCR 结合诱导的信号传导途径之一是钙池操纵的 Ca ²⁺进入 (SOCE)，它依赖于 Ca ²⁺通道 ORAI1 及其激活剂基质相互作用分子 (STIM) 1 和 2。最近的一项研究贝里等人。 [1] 报道称，缺乏 STIM1 和 STIM2 的 B 细胞无法存活和增殖，因为 SOCE 的废除会导致两个关键抗凋亡基因的表达受损以及 mTORC1 和 c-Myc 信号传导的激活减弱。通过 CD40 或 TLR9 的共刺激可以至少部分地绕过相关的 Ca ²⁺调节的 B 细胞存活和增殖检查点。这项研究为 SOCE 如何控制 B 细胞功能提供了重要的新见解。