ArticleNature communications2023
Toll-like receptor mediated inflammation directs B cells towards protective antiviral extrafollicular responses.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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.
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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
26 citing papers in PubMed, 31 citations in OpenAlex.
- Viral subversion of B-cell tolerance: mechanisms linking infection to autoimmunity.EMBO reports · 2026Review
- Autoantibodies to IL-1Ra and PGRN in severe COVID-19 are associated with inflammation-induced hyperphosphorylated antigen isoforms.Nature communications · 2026Article
- Multiple roads to IgE memory: A pluralistic model of IgE immunity.Cell reports · 2026Review
- Identification of Histone Deacetylase Inhibitor Targeting Type I Interferon and B Cell Abnormalities in Systemic Lupus Erythematosus.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- FNIP1 Modulates B Cell Receptor Signaling Strength by Coordinating Metabolism During Development.bioRxiv : the preprint server for biology · 2026Article
- Molecular mechanisms for direct sensing of virus-like antigens by B cells.International immunology · 2026Review
- Extrafollicular and other non-germinal center B cell responses.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Restoring B cell intrinsic tolerance to lupus autoimmunity: a rational strategy for lupus treatment.Frontiers in immunology · 2026Review
- PRDM1-mediated epigenetic and transcriptional repression mechanisms: a key hub in immune differentiation, tumor progression, and inflammatory responses.Frontiers in immunology · 2026Review
- Interferon regulatory factor 4 as a context-dependent regulator of inflammation: transcriptional and epigenetic control, skin diseases, and translational challenges.Frontiers in immunology · 2026Review
- B cell-intrinsic interleukin 17 receptor A signaling supports the establishment of chronic murine gammaherpesvirus 68 infection.Journal of virology · 2025Article
- Differential immune profiles in elderly patients with non-severe versus severe SARS-CoV-2 omicron variant infection: dysregulation of antibody responses and B-cell subsets.Immunity & ageing : I & A · 2025Article
- Immune response to platelet transfusions.Current opinion in hematology · 2025Review
- Extrafollicular B Cell Responses-Is One Tent Big Enough?Immunological reviews · 2025Review
- Ligand-receptor interactions induce and mediate regulatory functions of BATF3Science advances · 2025Article
- Antiviral nanomedicine: Advantages, mechanisms and advanced therapies.Bioactive materials · 2025Review
- T Cell Responses to Influenza Infections in Cattle.Viruses · 2025Review
- Deep Proteomics Analysis Unravels the Molecular Signatures of Tonsillar B Cells in PFAPA and OSAS in the Pediatric Population.International journal of molecular sciences · 2025Article
- Coordinated Regulation of Extrafollicular B Cell Responses by IL-12 and IFNγ.Immunological reviews · 2025Review
- Dysfunctional CD11cScience translational medicine · 2025Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Extrafollicular plasmablast responses (EFRs) are considered to generate antibodies of low affinity that offer little protection from infections. Paradoxically, high avidity antigen-B cell receptor engagement is thought to be the main driver of B cell differentiation, whether in EFRs or slower-developing germinal centers (GCs). Here we show that influenza infection rapidly induces EFRs, generating protective antibodies via Toll-like receptor (TLR)-mediated mechanisms that are both B cell intrinsic and extrinsic. B cell-intrinsic TLR signals support antigen-stimulated B cell survival, clonal expansion, and the differentiation of B cells via induction of IRF4, the master regulator of B cell differentiation, through activation of NF-kB c-Rel. Provision of sustained TLR4 stimulation after immunization shifts the fate of virus-specific B cells towards EFRs instead of GCs, prompting rapid antibody production and improving their protective capacity over antigen/alum administration alone. Thus, inflammatory signals act as B cell fate-determinants for the rapid generation of protective antiviral extrafollicular responses.
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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.