ArticleInfection and immunity2014
Role of Toll-like receptor 13 in innate immune recognition of group B streptococci.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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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Who cites it
25 citing papers in PubMed, 52 citations in OpenAlex.
- Amelioration of colitis through restored gut ecology using Christensenella intestinihominis AF73-05CM02 as a probiotic in mice.Communications biology · 2026Article
- Human neutrophils recognize group B streptococciFrontiers in immunology · 2026Article
- Immunization induces inflammation in the mouse heart during spaceflight.BMC genomics · 2025Article
- Role of endosomal toll-like receptors in immune sensing ofFrontiers in immunology · 2025Article
- Mass spectrometry-based proteomic exploration of diverse murine macrophage cellular models.Life science alliance · 2025Article
- Combining antibiotic with anti-TLR2/TLR13 therapy prevents brain pathology in pneumococcal meningitis.JCI insight · 2024Article
- Caspase-8 inhibition improves the outcome of bacterial infections in mice by promoting neutrophil activation.Cell reports. Medicine · 2023Article
- Immune Responses and Immunosuppressive Strategies for Adeno-Associated Virus-Based Gene Therapy for Treatment of Central Nervous System Disorders: Current Knowledge and Approaches.Human gene therapy · 2022Review
- TLR7 and TLR8 evolution in lagomorphs: different patterns in the different lineages.Immunogenetics · 2022Article
- Neutrophils discriminate live from dead bacteria by integrating signals initiated by Fprs and TLRs.The EMBO journal · 2022Article
- Toll-Like Receptor Evolution: Does Temperature Matter?Frontiers in immunology · 2022Article
- Aneuploid senescent cells activate NF-κB to promote their immune clearance by NK cells.EMBO reports · 2021Article
- Article
- Protein kinase D mediates inflammatory responses of human placental macrophages to Group B Streptococcus.American journal of reproductive immunology (New York, N.Y. : 1989) · 2019Article
- Legacy of the influenza pandemic 1918: Introduction.Biomedical journal · 2019Article
- The Chaperone UNC93B1 Regulates Toll-like Receptor Stability Independently of Endosomal TLR Transport.Immunity · 2018Article
- Group B Streptococcal Maternal Colonization and Neonatal Disease: Molecular Mechanisms and Preventative Approaches.Frontiers in pediatrics · 2018Review
- Group B Streptococci Induce Proinflammatory Responses via a Protein Kinase D1-Dependent Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Toll-Like Receptor 8 Is a Major Sensor of Group BFrontiers in immunology · 2017Article
- Long noncoding RNAs as regulators of Toll-like receptor signaling and innate immunity.Journal of leukocyte biology · 2016Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Murine Toll-like receptor 13 (TLR13), an endosomal receptor that is not present in humans, is activated by an unmethylated motif present in the large ribosomal subunit of bacterial RNA (23S rRNA). Little is known, however, of the impact of TLR13 on antibacterial host defenses. Here we examined the role of this receptor in the context of infection induced by the model pathogen group B streptococcus (GBS). To this end, we used bacterial strains masked from TLR13 recognition by virtue of constitutive expression of the ErmC methyltransferase, which results in dimethylation of the 23S rRNA motif at a critical adenine residue. We found that TLR13-mediated rRNA recognition was required for optimal induction of tumor necrosis factor alpha and nitrous oxide in dendritic cell and macrophage cultures stimulated with heat-killed bacteria or purified bacterial RNA. However, TLR13-dependent recognition was redundant when live bacteria were used as a stimulus. Moreover, masking bacterial rRNA from TLR13 recognition did not increase the ability of GBS to avoid host defenses and replicate in vivo. In contrast, increased susceptibility to infection was observed under conditions in which signaling by all endosomal TLRs was abolished, i.e., in mice with a loss-of-function mutation in the chaperone protein UNC93B1. Our data lend support to the conclusion that TLR13 participates in GBS recognition, although blockade of the function of this receptor can be compensated for by other endosomal TLRs. Lack of selective pressure by bacterial infections might explain the evolutionary loss of TLR13 in humans. However, further studies using different bacterial species are needed to prove this hypothesis.
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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.