ArticleArthritis & rheumatology (Hoboken, N.J.)2023
Interleukin-23 Regulates Inflammatory Osteoclastogenesis via Activation of CLEC5A(+) Osteoclast Precursors.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- The role of DAP12 in immune-related inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- The Role of Cytokines in Orthodontic Tooth Movement.International journal of molecular sciences · 2025Review
- Psoriatic arthritis: diagnosis, pathogenesis, and emerging therapies.Trends in molecular medicine · 2025Article
- Nephrectomy Induces Severe Bone Loss in Mice Expressing Constitutively Active TGFβ Receptor Type I.International journal of molecular sciences · 2025Article
- Pathogenesis of psoriatic arthritis: new insights from a bone marrow perspective.Current opinion in rheumatology · 2025Review
- Novel insights and recent progress in osteoimmunology.Trends in immunology · 2025Review
- Osteoclast Activation and Inflammatory Bone Diseases: Focusing on Receptors in Osteoclasts.Journal of inflammation research · 2025Review
- IL-23 induces CLEC5AJournal of autoimmunity · 2024Article
- Innate immune memory in inflammatory arthritis.Nature reviews. Rheumatology · 2023Review
- IL-27 attenuates IL-23 mediated inflammatory arthritis.Clinical immunology (Orlando, Fla.) · 2023Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveTo investigate the role of interleukin-23 (IL-23) in pathologic bone remodeling in inflammatory arthritis.
methodsIn this study we investigated the role of IL-23 in osteoclast differentiation and activation using in vivo gene transfer techniques in wild-type and myeloid DNAX-activation protein 12-associating lectin-1 (MDL-1)-deficient mice, and by performing in vitro and in vivo osteoclastogenesis assays using spectral flow cytometry, micro-computed tomography analysis, Western blotting, and immunoprecipitation.
resultsHerein, we show that IL-23 induces the expansion of a myeloid osteoclast precursor population and supports osteoclastogenesis and bone resorption in inflammatory arthritis. Genetic ablation of C-type lectin domain family member 5A, also known as MDL-1, prevents the induction of osteoclast precursors by IL-23 that is associated with bone destruction, as commonly observed in inflammatory arthritis. Moreover, osteoclasts derived from the bone marrow of MDL-1-deficient mice showed impaired osteoclastogenesis, and MDL-1
conclusionOur data show that IL-23 signaling regulates the availability of osteoclast precursors in inflammatory arthritis that could be effectively targeted for the treatment of inflammatory bone loss in inflammatory arthritis.
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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.