ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Regulation of TLR3 Activation by S100A9.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Ubiquitination by HRD1 is essential for TLR3 trafficking and its innate immune signaling.Nature communications · 2025Article
- The Chromosome 19 miRNA cluster guards trophoblasts against overacting innate immunity.Communications biology · 2025Article
- Involvement of nucleic acid-sensing toll-like receptors in human diseases and their controlling mechanisms.Journal of biomedical science · 2025Review
- Statin prevents cancer development in chronic inflammation by blocking interleukin 33 expression.Nature communications · 2024Article
- Genetic Susceptibility to Astrovirus Diarrhea in Bangladeshi Infants.Open forum infectious diseases · 2024Article
- Regulation of the nucleic acid-sensing Toll-like receptors.Nature reviews. Immunology · 2022Review
- Antimicrobial peptides: Defending the mucosal epithelial barrier.Frontiers in oral health · 2022Review
- PDLIM2 is highly expressed in Breast Cancer tumour-associated macrophages and is required for M2 macrophage polarization.Frontiers in oncology · 2022Article
- MicroRNA mimics can distort physiological microRNA effects on immune checkpoints by triggering an antiviral interferon response.RNA biology · 2022Article
- Review
- Intratumoral combination therapy with poly(I:C) and resiquimod synergistically triggers tumor-associated macrophages for effective systemic antitumoral immunity.Journal for immunotherapy of cancer · 2021Article
- Alarmin S100A9 restricts retroviral infection by limiting reverse transcription in human dendritic cells.The EMBO journal · 2021Article
- Establishment of an Endocytosis-Related Prognostic Signature for Patients With Low-Grade Glioma.Frontiers in genetics · 2021Article
- Molecular Events Involved in Influenza A Virus-Induced Cell Death.Frontiers in microbiology · 2021Review
- Ubiquitination of TLR3 by TRIM3 signals its ESCRT-mediated trafficking to the endolysosomes for innate antiviral response.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Lytic Cell Death Mechanisms in Human Respiratory Syncytial Virus-Infected Macrophages: Roles of Pyroptosis and Necroptosis.Viruses · 2020Article
- Loss of Function Genetic Screen Identifies ATM Kinase as a Positive Regulator of TLR3-Mediated NF-κB Activation.iScience · 2020Article
- Participation of Endosomes in Toll-Like Receptor 3 Transportation Pathway in Murine Astrocytes.Frontiers in cellular neuroscience · 2020Article
- Intranasal Delivery of Immunotherapeutic Nanoformulations for Treatment of Glioma Through in situ Activation of Immune Response.International journal of nanomedicine · 2020Article
- TLR5 is a new reporter for triple-negative breast cancer indicated by radioimmunoimaging and fluorescent staining.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Recognition of viral dsRNA by endosomal TLR3 activates innate immune response during virus infection. Trafficking of TLR3 to the endolysosomal compartment arising from fusion of late endosome (LE) with lysosome is required for recognition and detection of pathogen associated molecular patterns, which results in activation of the TLR3-dependent signaling cascade. Existing knowledge about the mechanism(s) and cellular factor(s) governing TLR3 trafficking is limited. In the current study, we identified intracellular S100A9 protein as a critical regulator of TLR3 trafficking. S100A9 was required for maturation of TLR3 containing early endosome (EE) into LE, the compartment that fuses with lysosome to form the endolysosomal compartment. A drastic reduction in cytokine production was observed in S100A9-knockout (KO) primary macrophages following RNA virus infection and treatment of cells with polyinosinic-polycytidylic acid (polyIC; a dsRNA mimetic that acts as a TLR3 agonist). Mechanistic studies revealed colocalization and interaction of S100A9 with TLR3 following polyIC treatment. S100A9-TLR3 interaction was critical for maturation of TLR3 containing EE into LE because TLR3 could not be detected in the LE of polyIC-treated S100A9-KO macrophages. Subsequently, TLR3 failed to colocalize with its agonist (i.e., biotin-labeled polyIC) in S100A9-deficient macrophages. The in vivo physiological role of S100A9 was evident from loss of cytokine production in polyIC-treated S100A9-KO mice. Thus, we identified intracellular S100A9 as a regulator of TLR3 signaling and demonstrated that S100A9 functions during pre-TLR3 activation stages by facilitating maturation of TLR3 containing EE into LE.
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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.