ArticleThe Journal of experimental medicine2024
Csk restrains BCR-mediated ROS production and contributes to germinal center selection and affinity maturation.
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 5 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Sex-specific autosomal susceptibility loci in systemic sclerosis: a genome-wide association study.The Lancet. Rheumatology · 2026Pooled it
- A guide to B cell metabolism.Nature reviews. Immunology · 2026Review
- Chronic infection perturbs the affinity hierarchy of antiviral B cells.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- B-cell peripheral tolerance: think dynamics beyond affinity.Frontiers in immunology · 2026Review
- Maf expression in B cells restricts reactive plasmablast and germinal center B cell expansion.Nature communications · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Compared with naïve B cells, the B cell receptor (BCR) signal in germinal center (GC) B cells is attenuated; however, the significance of this signaling attenuation has not been well defined. Here, to investigate the role of attenuation of BCR signaling, we employed a Csk mutant mouse model in which Csk deficiency in GC B cells resulted in augmentation of net BCR signaling with no apparent effect on antigen presentation. We found that Csk is required for GC maintenance and efficient antibody affinity maturation. Mechanistically, ROS-induced apoptosis was exacerbated concomitantly with mitochondrial dysfunction in Csk-deficient GC B cells. Hence, our data suggest that attenuation of the BCR signal restrains hyper-ROS production, thereby protecting GC B cells from apoptosis and contributing to efficient affinity maturation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.