ArticleProceedings of the National Academy of Sciences of the United States of America2024
Central tolerance shapes the neutralizing B cell repertoire against a persisting virus in its natural host.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Viral subversion of B-cell tolerance: mechanisms linking infection to autoimmunity.EMBO reports · 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 immunity to the Lassa virus glycoprotein is a correlate of vaccination-induced virus control in mice.Nature communications · 2026Article
- ImmunoMatch learns and predicts cognate pairing of heavy and light immunoglobulin chains.Nature methods · 2026Article
- Orf virus-based vectors induce potent germinal center B cell, Tfh cell, and CD8Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Polyclonal B cells acquire LCMV antigens in a GP1-dependent manner.PLoS pathogens · 2025Article
- Alterations in BCR heavy chain CDR3 repertoire characteristics in pediatric mycoplasma pneumoniae infection.Frontiers in cellular and infection microbiology · 2025Article
- Central tolerance shapes the neutralizing B cell repertoire against a persisting virus in its natural host.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
Viral mimicry of host cell structures has been postulated to curtail the B cell receptor (BCR) repertoire against persisting viruses through tolerance mechanisms. This concept awaits, however, experimental testing in a setting of natural virus-host relationship. We engineered mouse models expressing a monoclonal BCR specific for the envelope glycoprotein of lymphocytic choriomeningitis virus (LCMV), a naturally persisting mouse pathogen. When the heavy chain of the LCMV-neutralizing antibody KL25 was paired with its unmutated ancestor light chain, most B cells underwent receptor editing, a behavior reminiscent of autoreactive clones. In contrast, monoclonal B cells expressing the same heavy chain in conjunction with the hypermutated KL25 light chain did not undergo receptor editing but exhibited low levels of surface IgM, suggesting that light chain hypermutation had lessened KL25 autoreactivity. Upon viral challenge, these IgM
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