ArticleThe Journal of experimental medicine2024
STIM-mediated calcium influx regulates maintenance and selection of germinal center B cells.
Article in The Journal of experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Scalable context-dependent single-cell eQTL mapping reveals disease-relevant regulatory variation beyond static models.medRxiv : the preprint server for health sciences · 2026Article
- SERCA2 regulates Piezo1 channel activation and contributes to the cardiac function and baroreflex in mice.Acta pharmacologica Sinica · 2025Article
- Germinal Center B cells provide essential IL-1β signals to TFH cells via canonical NLRP3 inflammasome activity post influenza infection.PLoS pathogens · 2025Article
- New insights into the stromal interaction molecule 2 function and its impact on the immunomodulation of tumor microenvironment.Cell & bioscience · 2024Review
- B cells require DOCK8 to elicit and integrate T cell help when antigen is limiting.Science immunology · 2024Article
- Csk restrains BCR-mediated ROS production and contributes to germinal center selection and affinity maturation.The Journal of experimental medicine · 2024Article
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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