ArticleFrontiers in immunology2017
Co-Stimulation of BCR and Toll-Like Receptor 7 Increases Somatic Hypermutation, Memory B Cell Formation, and Secondary Antibody Response to Protein Antigen.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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
16 citing papers in PubMed, 24 citations in OpenAlex.
- Toll-like receptor 7/8 agonist stimulation rapidly skews the antibody repertoire of B cells in non-human primates.Frontiers in immunology · 2025Article
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- Tissue-specific sex differences in pediatric and adult immune cell composition and function.Frontiers in immunology · 2024Article
- Increased B Cell Understanding Puts Improved Vaccine Platforms Just Over the Horizon.Immune network · 2022Review
- Contribution of T- and B-cell intrinsic toll-like receptors to the adaptive immune response in viral infectious diseases.Cellular and molecular life sciences : CMLS · 2022Review
- B cell dysfunction in chronic hepatitis B virus infection.Liver research (Beijing, China) · 2021Review
- TLR7 Signaling Shapes and Maintains Antibody Diversity Upon Virus-Like Particle Immunization.Frontiers in immunology · 2021Article
- Toll-like receptors (TLRs): An old family of immune receptors with a new face in cancer pathogenesis.Journal of cellular and molecular medicine · 2021Review
- Influenza Vaccine-Induced CD4 Effectors Require Antigen Recognition at an Effector Checkpoint to Generate CD4 Lung Memory and Antibody Production.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Agonist and antagonist ligands of toll-like receptors 7 and 8: Ingenious tools for therapeutic purposes.European journal of medicinal chemistry · 2020Review
- TLR7 Is Critical for Anti-Viral Humoral Immunity to EV71 Infection in the Spinal Cord.Frontiers in immunology · 2020Article
- The Multiple Functions of B Cells in Chronic HBV Infection.Frontiers in immunology · 2020Review
- Toward a Functional Cure for Hepatitis B: The Rationale and Challenges for Therapeutic Targeting of the B Cell Immune Response.Frontiers in immunology · 2019Review
- RNA and Toll-Like Receptor 7 License the Generation of Superior Secondary Plasma Cells at Multiple Levels in a B Cell Intrinsic Fashion.Frontiers in immunology · 2019Article
- Biological sex affects vaccine efficacy and protection against influenza in mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Co-stimulation With TLR7 Agonist Imiquimod and Inactivated Influenza Virus Particles Promotes Mouse B Cell Activation, Differentiation, and Accelerated Antigen Specific Antibody Production.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The goal of immunization is to produce both a flood of antibodies to neutralize antigen and memory cells to accelerate the secondary response. To enhance the generation of memory B cells, we examined the effect of co-engaging BCR and toll-like receptor (TLR) 7 receptors by immunizing mice with a hapten-protein antigen, NP-CGG, and a ligand, R837 (imiquimod). During the early and late primary responses, there was no augmentation with R837 on the number of germinal center B cells or serum antibody. However, in the niche of germinal centers, R837 increased somatic hypermutation in the canonical V
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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.