Trial reportThe American journal of pathology2007
The Toll-like receptor adaptor proteins MyD88 and Mal/TIRAP contribute to the inflammatory and destructive processes in a human model of rheumatoid arthritis.
Trial report in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
75 citing papers in PubMed, 187 citations in OpenAlex.
- Editorial: Community series in targeting signalling pathways in inflammatory diseases, volume II.Frontiers in immunology · 2025Article
- Emerging interleukin-1 receptor-associated kinase 4 (IRAK4) inhibitors or degraders as therapeutic agents for autoimmune diseases and cancer.Acta pharmaceutica Sinica. B · 2024Review
- MyD88 dimerization inhibitor ST2825 targets the aggressiveness of synovial fibroblasts in rheumatoid arthritis patients.Arthritis research & therapy · 2023Article
- HMGB1 and Toll-like receptors: potential therapeutic targets in autoimmune diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- Therapeutic Potential of Targeting the NLRP3 Inflammasome in Rheumatoid Arthritis.Inflammation · 2023Review
- A novel IRAK4/PIM1 inhibitor ameliorates rheumatoid arthritis and lymphoid malignancy by blocking the TLR/MYD88-mediated NF-Acta pharmaceutica Sinica. B · 2023Article
- MiRNA-23a-5p is the biomarkers for gouty arthritis and promotes inflammation in rats of gouty arthritis via MyD88/NF-κB pathway by induction TLR2.Archives of rheumatology · 2022Article
- Toll-Like Receptor Signaling and Its Role in Cell-Mediated Immunity.Frontiers in immunology · 2022Review
- Is there an Inflammation Role for MYD88 in Rheumatoid Arthritis?Inflammation · 2021Article
- Microbiota-Derived Metabolites, Indole-3-aldehyde and Indole-3-acetic Acid, Differentially Modulate Innate Cytokines and Stromal Remodeling Processes Associated with Autoimmune Arthritis.International journal of molecular sciences · 2021Article
- Inhibiting TLR7 Expression in the Retinal Pigment Epithelium Suppresses Experimental Autoimmune Uveitis.Frontiers in immunology · 2021Article
- The One That Got Away: How Macrophage-Derived IL-1β Escapes the Mycolactone-Dependent Sec61 Blockade in Buruli Ulcer.Frontiers in immunology · 2021Article
- Contribution of Toll-Like Receptors and the NLRP3 Inflammasome in Rheumatoid Arthritis Pathophysiology.ImmunoTargets and therapy · 2021Review
- Paradoxical Roles of the MAL/Tirap Adaptor in Pathologies.Frontiers in immunology · 2020Review
- The Mechanism of Aureusidin in Suppressing Inflammatory Response in Acute Liver Injury by Regulating MD2.Frontiers in pharmacology · 2020Article
- Toll-like receptor 4 inhibition prevents autoimmune diabetes in NOD mice.Scientific reports · 2019Article
- Platelets: emerging facilitators of cellular crosstalk in rheumatoid arthritis.Nature reviews. Rheumatology · 2019Review
- Ameliorating effects of Gö6976, a pharmacological agent that inhibits protein kinase D, on collagen-induced arthritis.PloS one · 2019Article
- Small-Molecule TLR8 Antagonists via Structure-Based Rational Design.Cell chemical biology · 2018Article
- Novel insights into the role of inflammasomes in autoimmune and metabolic rheumatic diseases.Rheumatology international · 2018Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The widespread distribution of Toll-like receptors (TLRs) and their ligands raises the question whether they contribute to the production of inflammatory and tissue destructive molecules in rheumatoid arthritis (RA). We examined the expression and function of TLR2 and TLR4 and their downstream signaling adaptors MyD88 and Mal/TIRAP in synovial membrane cultures from RA tissue. Both TLR2 and TLR4 were detected by flow cytometry, and stimulation with TLR2 and TLR4 ligands augmented the spontaneous production of tumor necrosis factor-alpha, interleukin (IL)-6, and IL-8, indicating that TLR2 and TLR4 are functional in these cultures. In addition, overexpression of dominant-negative forms of MyD88 and Mal/TIRAP significantly down-regulated the spontaneous production of cytokines tumor necrosis factor-alpha, IL-6, and vascular endothelial growth factor, and enzymes MMP-1, MMP-2, MMP-3, and MMP-13 in RA synovial membrane cell cultures. Because TLR2 and TLR4 require both MyD88 and Mal/TIRAP for signaling, this study suggests that TLR function may regulate the expression of these factors in the RA synovium. Conditioned media from synovial membrane cell cultures stimulated human macrophages in a MyD88- and Mal-dependent manner, suggesting the release of a TLR ligand(s) from these cells. Thus, TLRs not only protect against infection but may also promote the inflammatory and destructive process in RA.
Indexed as
Identifiers
What OpenQuestion holds
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.