ArticleThe Journal of clinical investigation2005
IL-1 mediates TNF-induced osteoclastogenesis.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 345 papers.
What it found
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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.
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.
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Who cites it
345 citing papers in PubMed, 669 citations in OpenAlex.
- Interleukin-9 Facilitates Osteoclastogenesis in Rheumatoid Arthritis.International journal of molecular sciences · 2021Trial
- Review
- Bone Tumor Microenvironment Is Associated with Meningioma Enlargement and Inflammatory Transcriptional States: A Candidate Role for Macrophage-Derived IL-1β.Biomedicines · 2026Article
- Heme Oxygenase-1 in Bone Remodeling: Molecular Mechanisms and Therapeutic Implications.Biomolecules · 2026Review
- Multifactorial Regulation of Inflammatory Bone Loss in Chronic Inflammatory and Immune-Associated Disorders: Osteoimmune Mechanisms and Translational Prospects of Natural Small Molecules.Calcified tissue international · 2026Review
- Brain-bone Crosstalk after Neurotrauma: Dual Effects of Traumatic Brain Injury on Skeletal Remodeling.Current osteoporosis reports · 2026Review
- Punicalagin with anti-inflammatory activities affects Brd-4 mediated chromatin remodeling for attenuating inflammatory osteolysis.Scientific reports · 2026Article
- Narrative review on the development of multi-target pharmacological agents for the management of rheumatoid arthritis.Inflammopharmacology · 2026Review
- Mechanisms of osteoclast activation in inflammatory bone loss in rheumatoid arthritis.Nature reviews. Rheumatology · 2026Review
- Role of Cytokines in Bone Diseases and Their Therapeutic Application.ImmunoTargets and therapy · 2026Review
- CX3CR1 and CCR2: dynamic myeloid cell states across inflammatory diseases with implications for oral health and disease.Frontiers in immunology · 2026Review
- The mechanism of action and therapeutic potential of macrophages in osteoporosis: from polarization balance to targeted regulation.Frontiers in immunology · 2026Review
- Osteoimmunology: interactions of the bone and immune system.Frontiers in immunology · 2026Review
- Crosstalk Between Hematopoietic and Mesenchymal Cells in Bone and Tooth Immune Response.Advances in experimental medicine and biology · 2026Review
- RANKL-convergent osteoimmune network framework in osteoporosis: integrating macrophage activation, T-cell imbalance, and cytokine crosstalk.Frontiers in immunology · 2026Review
- The impact of alpha-lipoic acid treatment on various mediators of inflammatory and immune responses in a murine arthritis model.Inflammopharmacology · 2025Article
- Shaping Orthodontics of the Future: Concepts and Implications from a Cellular and Molecular Perspective.International journal of molecular sciences · 2025Review
- 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
- Effect of 3D-printing assisted micro-osteoperforations on the rate of canine retraction: a clinical investigation.BMC oral health · 2025Article
- Spinal implant wear particles: Generation, characterization, biological impacts, and future considerations.iScience · 2025Review
285 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
5 authors at 1 institution in 1 country.
Funding
Abstract
TNF-induced receptor activator NF-kappaB ligand (RANKL) synthesis by bone marrow stromal cells is a fundamental component of inflammatory osteolysis. We found that this process was abolished by IL-1 receptor antagonist (IL-1Ra) or in stromal cells derived from type I IL-1 receptor-deficient (IL-1RI-deficient) mice. Reflecting sequential signaling of the cytokines TNF and IL-1, TNF induces stromal cell expression of IL-1 and IL-1RI. These data suggest that TNF regulates RANKL expression via IL-1, and, therefore, IL-1 plays a role in TNF-induced periarticular osteolysis. Consistent with this posture, TNF-stimulated osteoclastogenesis in cultures consisting of WT marrow macrophages and stromal cells exposed to IL-1Ra or in cocultures established with IL-1RI-deficient stromal cells was reduced approximately 50%. The same magnitude of osteoclast inhibition occurred in IL-1RI-deficient mice following TNF administration in vivo. Like TNF, IL-1 directly targeted osteoclast precursors and promoted the osteoclast phenotype in a TNF-independent manner in the presence of permissive levels of RANKL. IL-1 is able to induce RANKL expression by stromal cells and directly stimulate osteoclast precursor differentiation under the aegis of p38 MAPK. Thus, IL-1 mediates the osteoclastogenic effect of TNF by enhancing stromal cell expression of RANKL and directly stimulating differentiation of osteoclast precursors.
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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.