ArticleJBMR plus2024
Targeting the osteoclastogenic cytokine IL-9 as a novel immunotherapeutic strategy in mitigating inflammatory bone loss in post-menopausal osteoporosis.
Article in JBMR plus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Article
- Review
- Bone and Infections: An Osteoimmunological Interplay.International journal of molecular sciences · 2026Review
- Perioperative inflammatory cytokines nursing screening test indicate the link between dysregulated lipid metabolism and reduced bone mineral density in obese osteoporosis patients: a retrospective study.BMC musculoskeletal disorders · 2026Article
- Roles of gut metabolites on bone mineralization and remodeling: impact of metabolic dysregulation on the gut-immune-bone axis.Frontiers in endocrinology · 2026Review
- Diallyl Disulfide Mitigates LPS-Induced Inhibition of Osteogenic Differentiation and Alleviates Inflammatory Bone Loss via PI3K/AKT Signaling Pathway.Drug design, development and therapy · 2026Article
- Role of Cytokines in Bone Diseases and Their Therapeutic Application.ImmunoTargets and therapy · 2026Review
- IL-34 as a Novel Mediator Linking Vitamin D Deficiency with Osteoporosis and Knee Osteoarthritis.International journal of molecular sciences · 2025Article
- Causal effects and mediation pathways of circulating plasma proteins on osteoporosis: a two-sample and two-step Mendelian randomization study.Clinical proteomics · 2025Article
- Research Trends in Immunomodulatory Therapy for Postmenopausal Osteoporosis: A Bibliometric Analysis.Orthopaedic surgery · 2025Review
- Oxidative stress and inflammation: roles in osteoporosis.Frontiers in immunology · 2025Review
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Authors and funding
12 authors.
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Abstract
Recent discoveries have established the pivotal role of IL-9-secreting immune cells in a wide spectrum of inflammatory and autoimmune diseases. However, little is known about how IL-9 contributes to the etiology of inflammatory bone loss in PMO. We observed that IL-9 has a pathological impact on inflammatory bone loss in ovariectomized (Ovx) mice. Our in vivo temporal kinetics analysis revealed that estrogen deprivation enhanced the production of IL-9 from Th cells (majorly Th9 and Th17). Both our ex vivo and in vivo studies corroborated these findings in Ovx mice, as estrogen diminishes the potential of Th9 cells to produce IL-9. Mechanistically, Th9 cells in an IL-9-dependent manner enhance osteoclastogenesis and thus could establish themselves as a novel osteoclastogenic Th cell subset. Therapeutically neutralizing/blocking IL-9 improves bone health by inhibiting the differentiation and function of osteoclasts, Th9, and Th17 cells along with maintaining gut integrity in Ovx mice. Post-menopausal osteoporotic patients have increased IL-9-secreting Th9 cells, which may suggest a potential role for IL-9 in the development of osteoporosis. Collectively, our study identifies IL-9-secreting Th9 cells as a driver of bone loss with attendant modulation of gut-immune-bone axis, which implies IL-9-targeted immunotherapies as a potential strategy for the management and treatment of inflammatory bone loss observed in PMO.
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