ArticleJournal of immunology (Baltimore, Md. : 1950)2009
Heat shock protein 96 is elevated in rheumatoid arthritis and activates macrophages primarily via TLR2 signaling.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 156 citations in OpenAlex.
- Considering evolved heat tolerance helps predict the immunological consequences of climate change.Seminars in immunopathology · 2026Review
- Spatial and functional characterization of ER stress proteins links fibroblast plasticity and proliferative processes in human osteoarthritic synovitis.Cell death and differentiation · 2026Article
- Neutrophil extracellular traps promote macrophage activation through Toll-like receptor engagement and PKA and NF-kB signaling pathways.Cell communication and signaling : CCS · 2026Article
- ER-resident proteins are key players in cartilage and bone homeostasis.Frontiers in cell and developmental biology · 2025Review
- Underpinning Endogeneous Damp EDA-Fibronectin in the Activation of Molecular Targets of Rheumatoid Arthritis and Identifcation of its Effective Inhibitors by Computational Methods.Applied biochemistry and biotechnology · 2023Article
- The Role of Extracellular Heat Shock Proteins in Cardiovascular Diseases.Biomedicines · 2023Review
- Electroacupuncture Alleviates Pain Responses and Inflammation in Collagen-Induced Arthritis Rats via Suppressing the TLR2/4-MyD88-NF-Evidence-based complementary and alternative medicine : eCAM · 2023Article
- Corrected and Republished from: "A Novel, Multiple-Antigen Pneumococcal Vaccine Protects against LethalInfection and immunity · 2022Article
- Glycoprotein 96 in Peritoneal Dialysis Effluent-Derived Extracellular Vesicles: A Tool for Evaluating Peritoneal Transport Properties and Inflammatory Status.Frontiers in immunology · 2022Article
- Rs41291957 polymorphism in the promoter region of microRNA‑143 serves as a prognostic biomarker for patients with intracranial hemorrhage.Molecular medicine reports · 2021Article
- Contribution of Toll-Like Receptors and the NLRP3 Inflammasome in Rheumatoid Arthritis Pathophysiology.ImmunoTargets and therapy · 2021Review
- Proteins involved in the endoplasmic reticulum stress are modulated in synovitis of osteoarthritis, chronic pyrophosphate arthropathy and rheumatoid arthritis, and correlate with the histological inflammatory score.Scientific reports · 2020Article
- Anti-inflammatory effects of naproxen sodium on human osteoarthritis synovial fluid immune cells.Osteoarthritis and cartilage · 2020Article
- Common innate pathways to autoimmune disease.Clinical immunology (Orlando, Fla.) · 2020Review
- Roles of Interactions Between Toll-Like Receptors and Their Endogenous Ligands in the Pathogenesis of Systemic Juvenile Idiopathic Arthritis and Adult-Onset Still's Disease.Frontiers in immunology · 2020Review
- A Novel, Multiple-Antigen Pneumococcal Vaccine Protects against LethalInfection and immunity · 2019Article
- Identification of a TLR2 Inhibiting Wheat Hydrolysate.Molecular nutrition & food research · 2018Article
- Damage-Associated Molecular Patterns in Inflammatory Diseases.Immune network · 2018Review
- Association of HSP90B1 genetic polymorphisms with efficacy of glucocorticoids and improvement of HRQoL in systemic lupus erythematosus patients from Anhui Province.American journal of clinical and experimental immunology · 2018Article
- The Role of Macrophages in the Response to TNF Inhibition in Experimental Arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Macrophages are important mediators of chronic inflammation and are prominent in the synovial lining and sublining of patients with rheumatoid arthritis (RA). Recently, we demonstrated increased TLR2 and TLR4 expression and increased response to microbial TLR2 and TLR4 ligands in macrophages from the joints of RA. The current study characterized the expression of the 96-kDa heat shock glycoprotein (gp96) in the joints of RA and its role as an endogenous TLR ligand to promote innate immunity in RA. gp96 was increased in RA compared with osteoarthritis and arthritis-free control synovial tissues. The expression of gp96 strongly correlated with inflammation and synovial lining thickness. gp96 was increased in synovial fluid from the joints of RA compared with disease controls. Recombinant gp96 was a potent activator of macrophages and the activation was mediated primarily through TLR2 signaling. The cellular response to gp96 was significantly stronger with RA synovial macrophages compared with peripheral blood monocytes from RA or healthy controls. The transcription of TLR2, TNF-alpha, and IL-8, but not TLR4, was significantly induced by gp96, and the induction was significantly greater in purified RA synovial macrophages. The expression of TLR2, but not TLR4, on synovial fluid macrophages strongly correlated with the level of gp96 in the synovial fluid. The present study documents the potential role of gp96 as an endogenous TLR2 ligand in RA and provides insight into the mechanism by which gp96 promotes the chronic inflammation of RA, identifying gp96 as a potential new therapeutic target.
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