ReviewFrontiers in immunology2019
Regulation of Immune Responses and Chronic Inflammation by Fibroblast-Like Synoviocytes.
Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
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Who cites it
114 citing papers in PubMed, 189 citations in OpenAlex.
- Cellular crosstalk and signaling networks in the rheumatoid arthritis synovial microenvironment.Journal of translational medicine · 2026Review
- Hyaluronic acid microneedle patch for transdermal delivery of naringin-loaded PEGylated terpesomes in a rat model of rheumatoid arthritis: Modulation TGF-β1, oxidative stress, and inflammation.International journal of pharmaceutics: X · 2026Article
- Iguratimod ameliorated collagen-induced arthritis by suppressing TNF-α/NF-κB signaling pathway and enhancing lymphangiogenesis in a murine model.Scientific reports · 2026Article
- Article
- Genetic alternative splicing regulation mapping of cartilage and synovium reveals tissue-specific mechanisms of joint-related traits.Nature communications · 2026Article
- The effect of walnut consumption on the peripheral blood mononuclear cell transcriptome.Genes & nutrition · 2026Article
- Fibroblasts as Immunological Sentinels in Cutaneous Inflammation: A Review.Journal of clinical medicine · 2026Review
- Combination of Chenpi and Banxia alleviates synovial inflammation in a rat model of rheumatoid arthritis by targeting the JNK/AP-1 signaling pathway.Frontiers in immunology · 2026Article
- Macrophage IL-1β turns meningeal fibroblasts into inflammatory amplifiers in pneumococcal infection.Frontiers in immunology · 2026Article
- NR1D1-Mediated Suppression of JAK1/STAT3 Signaling Contributes to the Therapeutic Effects of Triptolide in Rheumatoid Arthritis.Mediators of inflammation · 2026Article
- Tumor necrosis factor alpha triggers mitochondrial dysfunction and ROS-driven cytokine amplification in bovine fibroblast-like synoviocytes.Frontiers in veterinary science · 2026Article
- IL-34-mediated fibroblast-like synoviocyte-macrophage crosstalk drives bone erosion in rheumatoid arthritis through RANKL-dependent osteoclastogenesis.Frontiers in immunology · 2026Article
- Bone marrow mesenchymal stem cell-derived exosomes improve pyroptosis and mitochondrial integrity through miR-515-5p-mediated TLR4/NLRP3/GSDMD axis in rheumatoid arthritis.Arthritis research & therapy · 2025Article
- A CCL5Cell & bioscience · 2025Article
- Targeting GM-CSF in Rheumatoid Arthritis: Advances in Cytokine-Directed Immunotherapy and Clinical Implications.Life (Basel, Switzerland) · 2025Review
- Function of p53 in angiogenesis and oxidative stress in rheumatoid arthritis.Clinical and experimental medicine · 2025Review
- RNA-seq Based Transcriptome Analysis Reveals Role of Myoglobin in Rheumatoid Arthritis.Inflammation · 2025Article
- Deciphering the role of ERK and PI3K/Akt as crosstalk pathways between fibroblast-like synoviocytes and osteoclasts; novel therapeutic approach for rheumatoid arthritis.Molecular biology reports · 2025Review
- Advances in Regenerative Therapies for Inflammatory Arthritis: Exploring the Potential of Mesenchymal Stem Cells and Extracellular Vesicles.International journal of molecular sciences · 2025Review
- Unveiling the Therapeutic Potential: Targeting Fibroblast-like Synoviocytes in Rheumatoid Arthritis.Expert reviews in molecular medicine · 2025Review
54 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synovial tissue is a membranous non-immune organ lining joint cavities where it supports local immune responses, and functions directly and indirectly in joint destruction due to chronic inflammatory diseases such as rheumatoid arthritis (RA). Fibroblast-like synoviocytes (FLS), the dominant non-immune cells of synovial tissues, mainly contribute to joint destruction via multiple mechanisms. In RA, FLS respond to endogenous ligands of pattern recognition receptors (PRRs) and inflammatory cytokines as non-immune cells. In addition, FLS aid in the activation of immune responses by interacting with immune cells and by supporting ectopic lymphoid-like structure (ELS) formation in synovial tissues. Moreover, FLS directly cause the pathogenicity of RA i.e., joint deformities. Here, we describe new findings and review the mechanisms underlying the regulation of immune reactions by non-immune FLS and their roles in inflammatory diseases such as RA.
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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.