ArticleFrontiers in immunology2017
Interleukin-7 Induces Osteoclast Formation
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 32 citations in OpenAlex.
- Cytokine Regulation of the Bone Pre- and Metastatic Niches: Implications for Breast Cancer Dormancy.Cells · 2026Review
- Spatial transcriptomic atlas of aggressive osteosarcomas reveals shared immune landscape and targetable surface markers.Nature communications · 2026Article
- Role of Cytokines in Bone Diseases and Their Therapeutic Application.ImmunoTargets and therapy · 2026Review
- Mesenchymal Stromal Cell-Derived Extracellular Vesicles as a Therapeutic Treatment for Osteosarcopenia: Crosstalk Among Neurons, Muscle, and Bone.International journal of molecular sciences · 2025Article
- Deficiency of IL-7R attenuates abdominal aortic aneurysms in mice by inhibiting macrophage polarization towards M1 phenotype through the NF-κB pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Unraveling the link between metabolic dysfunction-associated steatotic liver disease and osteoporosis: a bridging function of gut microbiota.Frontiers in endocrinology · 2025Review
- Article
- Identification and validation of immune-related genes in osteoarthritic synovial fibroblasts.Heliyon · 2024Article
- Osteoimmunology: The Crosstalk between T Cells, B Cells, and Osteoclasts in Rheumatoid Arthritis.International journal of molecular sciences · 2024Review
- The reciprocity of skeletal muscle and bone: an evolving view from mechanical coupling, secretory crosstalk to stem cell exchange.Frontiers in physiology · 2024Review
- Effects of circulating inflammatory proteins on osteoporosis and fractures: evidence from genetic correlation and Mendelian randomization study.Frontiers in endocrinology · 2024Article
- Inflammatory Processes Affecting Bone Health and Repair.Current osteoporosis reports · 2023Review
- The Notch1 signaling pathway directly modulates the human RANKL-induced osteoclastogenesis.Scientific reports · 2023Article
- Mechanistic insight of interleukin-9 induced osteoclastogenesis.Immunology · 2023Article
- The effect of cytokines on osteoblasts and osteoclasts in bone remodeling in osteoporosis: a review.Frontiers in immunology · 2023Review
- Review
- Significance of IL-7 and IL-7R in RA and autoimmunity.Autoimmunity reviews · 2022Review
- Roles of the RANKL-RANK Axis in Immunity-Implications for Pathogenesis and Treatment of Bone Metastasis.Frontiers in immunology · 2022Review
- Age-related accumulation of advanced oxidation protein products promotes osteoclastogenesis through disruption of redox homeostasis.Cell death & disease · 2021Article
- Novel Majeed Syndrome-Causing LPIN2 Mutations Link Bone Inflammation to Inflammatory M2 Macrophages and Accelerated Osteoclastogenesis.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-7 (IL-7), which is required for the development and survival of T cells in the thymus and periphery, plays a role in joint destruction. However, it remains unclear how IL-7 affects osteoclast formation. Thus, we investigated the mechanism by which IL-7 induced osteoclast formation through IL-7 receptor α (IL-7Rα) in osteoclast precursors. We cultured peripheral blood mononuclear cells or synovial fluid mononuclear cells with IL-7 in the presence or absence of an appropriate inhibitor to analyze osteoclast formation. We also constructed IL-7Rα-expressing RAW264.7 cells to uncover the mechanism(s) by which IL-7 induced osteoclast formation differed from that of receptor activator of nuclear factor κB ligand (RANKL). We found that IL-7 induced osteoclast formation of human monocytes from peripheral blood or synovial fluid in a RANKL-independent and a signal transducer and activator of transcription 5 (STAT5)-dependent manner. IL-7-induced osteoclasts had unique characteristics, such as small, multinucleated tartrate-resistant acid phosphatase positive cells and no alterations even when RANKL was added after IL-7 pretreatment. RAW264.7 cells, if overexpressing IL-7Rα, also were able to differentiate into osteoclasts by IL-7 through a STAT5 signaling pathway. Furthermore, IL-7-induced osteoclast formation was repressed by inhibitors of the IL-7R signaling molecules Janus kinase and STAT5. Our findings demonstrate that IL-7 is a truly osteoclastogenic factor, which may induce osteoclast formation
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