| First Author | Yada Y | Year | 2024 |
| Journal | J Exp Med | Volume | 221 |
| Issue | 1 | PubMed ID | 37902601 |
| Mgi Jnum | J:342114 | Mgi Id | MGI:7546742 |
| Doi | 10.1084/jem.20222178 | Citation | Yada Y, et al. (2024) STIM-mediated calcium influx regulates maintenance and selection of germinal center B cells. J Exp Med 221(1) |
| abstractText | Positive selection of high-affinity germinal center (GC) B cells is driven by antigen internalization through their B cell receptor (BCR) and presentation to follicular helper T cells. However, the requirements of BCR signaling in GC B cells remain poorly understood. Store-operated Ca2+ entry, mediated by stromal interacting molecule 1 (STIM1) and STIM2, is the main Ca2+ influx pathway triggered by BCR engagement. Here, we showed that STIM-deficient B cells have reduced B cell competitiveness compared with wild-type B cells during GC responses. B cell-specific deletion of STIM proteins decreased the number of high-affinity B cells in the late phase of GC formation. STIM deficiency did not affect GC B cell proliferation and antigen presentation but led to the enhancement of apoptosis due to the impaired upregulation of anti-apoptotic Bcl2a1. STIM-mediated activation of NFAT was required for the expression of Bcl2a1 after BCR stimulation. These findings suggest that STIM-mediated survival signals after antigen capture regulate the optimal selection and maintenance of GC B cells. |
