ArticleThe Journal of experimental medicine2020
Transmembrane TNF drives osteoproliferative joint inflammation reminiscent of human spondyloarthritis.
Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Macrophage-driven pathological ossification of the posterior longitudinal ligament: mechanistic insights and therapeutic opportunities.Bone research · 2026Review
- From screening to treatment:Microbiology spectrum · 2026Article
- Novel Sonoguided Digital Palpation and Hydrodissection for Sural Nerve Dysfunction Mimicking Achilles Tendinopathy in a Psoriasis Patient.Diagnostics (Basel, Switzerland) · 2025Article
- Development of a Mouse Model of Enthesis-Specific NF-κB Activation.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Pathogenesis of psoriatic arthritis: new insights from a bone marrow perspective.Current opinion in rheumatology · 2025Review
- Beyond inflammation: the molecular basis of bone remodeling in axial spondyloarthritis and psoriatic arthritis.Frontiers in immunology · 2025Review
- Updates on ankylosing spondylitis: pathogenesis and therapeutic agents.Journal of rheumatic diseases · 2023Review
- Inflammatory Cytokines in Psoriatic Arthritis: Understanding Pathogenesis and Implications for Treatment.International journal of molecular sciences · 2023Review
- CXCL12/CXCR4-Rac1-mediated migration of osteogenic precursor cells contributes to pathological new bone formation in ankylosing spondylitis.Science advances · 2022Article
- Splenic Architecture and Function Requires Tight Control of Transmembrane TNF Expression.International journal of molecular sciences · 2022Article
- Dual Blockade of TNF and IL-17A Inhibits Inflammation and Structural Damage in a Rat Model of Spondyloarthritis.International journal of molecular sciences · 2022Article
- Potent anti-inflammatory activity of the lectin-like domain of TNF in joints.Frontiers in immunology · 2022Article
- B Cell Involvement in the Pathogenesis of Ankylosing Spondylitis.International journal of molecular sciences · 2021Review
- Tumor Necrosis Factor Inhibitors Reduce Spinal Radiographic Progression in Patients With Radiographic Axial Spondyloarthritis: A Longitudinal Analysis From the Alberta Prospective Cohort.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
- Lessons on SpA pathogenesis from animal models.Seminars in immunopathology · 2021Review
- The Role of the IL-23/IL-17 Axis in Disease Initiation in Spondyloarthritis: Lessons Learned From Animal Models.Frontiers in immunology · 2021Review
- CD27Frontiers in immunology · 2021Article
- Inflammatory Foot Involvement in Spondyloarthritis: From Tarsitis to Ankylosing Tarsitis.Frontiers in medicine · 2021Review
- Ectopic bone formation and systemic bone loss in a transmembrane TNF-driven model of human spondyloarthritis.Arthritis research & therapy · 2020Article
- IL-23 Inhibition in Ankylosing Spondylitis: Where Did It Go Wrong?Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TNF plays a key role in immune-mediated inflammatory diseases including rheumatoid arthritis (RA) and spondyloarthritis (SpA). It remains incompletely understood how TNF can lead to different disease phenotypes such as destructive peripheral polysynovitis in RA versus axial and peripheral osteoproliferative inflammation in SpA. We observed a marked increase of transmembrane (tm) versus soluble (s) TNF in SpA versus RA together with a decrease in the enzymatic activity of ADAM17. In contrast with the destructive polysynovitis observed in classical TNF overexpression models, mice overexpressing tmTNF developed axial and peripheral joint disease with synovitis, enthesitis, and osteitis. Histological and radiological assessment evidenced marked endochondral new bone formation leading to joint ankylosis over time. SpA-like inflammation, but not osteoproliferation, was dependent on TNF-receptor I and mediated by stromal tmTNF overexpression. Collectively, these data indicate that TNF can drive distinct inflammatory pathologies. We propose that tmTNF is responsible for the key pathological features of SpA.
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Registered trials
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