ArticleArthritis & rheumatology (Hoboken, N.J.)2016
Identification of a Novel Toll-like Receptor 7 Endogenous Ligand in Rheumatoid Arthritis Synovial Fluid That Can Provoke Arthritic Joint Inflammation.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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
59 citing papers in PubMed, 101 citations in OpenAlex.
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- Extracellular Vesicle Protein and MiRNA Signatures as Biomarkers for Post-Infectious ME/CFS Patients.International journal of molecular sciences · 2026Article
- Exosomal miRNAs involvement in pathogenesis, diagnosis, and treatment of rheumatoid arthritis.Heliyon · 2025Review
- The status and hotspot analysis of research on extracellular vesicles and osteoarthritis: a bibliometric analysis.Frontiers in pharmacology · 2025Review
- miR-574-5p in epigenetic regulation and Toll-like receptor signaling.Cell communication and signaling : CCS · 2024Review
- Cell damage shifts the microRNA content of small extracellular vesicles into a Toll-like receptor 7-activating cargo capable to propagate inflammation and immunity.Cell communication and signaling : CCS · 2024Article
- Yin-Yang: two sides of extracellular vesicles in inflammatory diseases.Journal of nanobiotechnology · 2024Review
- The miR-29-3p family suppresses inflammatory osteolysis.Journal of cellular physiology · 2024Article
- Targeting TLR Signaling Cascades in Systemic Lupus Erythematosus and Rheumatoid Arthritis: An Update.Biomedicines · 2024Article
- Diagnostic and Therapeutic Roles of Extracellular Vesicles and Their Enwrapped ncRNAs in Rheumatoid Arthritis.Journal of inflammation research · 2024Review
- MicroRNAs as Key Regulators in RA and SLE: Insights into Biological Functions.Current pharmaceutical design · 2024Review
- Comprehensive overview of microRNA function in rheumatoid arthritis.Bone research · 2023Review
- The internal dose makes the poison: higher internalization of polystyrene particles induce increased perturbation of macrophages.Frontiers in immunology · 2023Article
- Elucidating a fresh perspective on the interplay between exosomes and rheumatoid arthritis.Frontiers in cell and developmental biology · 2023Review
- Differential Expression Profiles of Plasma Exosomal microRNAs in Rheumatoid Arthritis.Journal of inflammation research · 2023Article
- Antiviral Innate Immune Responses in Autoimmunity: Receptors, Pathways, and Therapeutic Targeting.Biomedicines · 2022Review
- Inhibition of IRAK4 dysregulates SARS-CoV-2 spike protein-induced macrophage inflammatory and glycolytic reprogramming.Cellular and molecular life sciences : CMLS · 2022Article
- Update on the role of extracellular vesicles in rheumatoid arthritis.Expert reviews in molecular medicine · 2022Review
- Myeloid Responses to Extracellular Vesicles in Health and Disease.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveLevels of Toll-like receptor 7 (TLR-7) are elevated in rheumatoid arthritis (RA), but the impact on RA is unknown because the endogenous ligand for TLR-7 has not been identified. The aim of this study was to identify a TLR-7 endogenous ligand and to determine its role in the pathogenesis of RA.
methodsThe presence of an endogenous TLR-7 ligand, microRNA let-7b (miR-let-7b), was examined by real-time polymerase chain reaction (PCR) analysis. Using RA knockdown cells, TLR-7-knockout mice, or antagonist, the specificity of miR-let-7b as a potential ligand for TLR-7 was tested. The mechanism by which ligation of miR-let-7b to TLR-7 promotes disease was investigated in RA myeloid cells by real-time PCR, enzyme-linked immunosorbent assay, and fluorescence-activated cell sorting. We also established the effect of ectopic miR-let-7b expression on arthritic joint inflammation.
resultsWe found that a TLR-7 endogenous ligand resides mainly in RA synovial fluid macrophages. The GU-rich domain in miR-let-7b was found to be essential for TLR-7 ligation, since miR-147, the positive control for GU, was able to stimulate TLR-7+ myeloid cells, whereas miR-124, the negative, non-GU, control, was not. We demonstrated that miR-let-7b or exosomes containing miR-let-7b could transform the RA and/or mouse naive or antiinflammatory macrophages into inflammatory M1 macrophages via TLR-7 ligation. Consistently, we showed that miR-let-7b provokes arthritis by remodeling naive myeloid cells into M1 macrophages via TLR-7 ligation, since joint swelling and M1 macrophages are absent in TLR-7-deficient mice.
conclusionThe results of this study underscore the importance of miR-let-7b ligation to TLR-7 in the joint during the effector phase of RA.
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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.