ArticlePloS one2013
The newly discovered cytokine IL-34 is expressed in gingival fibroblasts, shows enhanced expression by pro-inflammatory cytokines, and stimulates osteoclast differentiation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 99 citations in OpenAlex.
- Roles of IL-34 in neurological diseases: neuroprotection, inflammatory regulation, and myeloid plasticity.Frontiers in immunology · 2026Review
- Sparse dimensionality reduction for analyzing single-cell-resolved interactions.Bioinformatics advances · 2026Article
- CSF1R inhibitor (PLX3397) alleviates experimental periodontitis by reducing macrophage senescence through the PI3K/AKT/FOXO1 signaling pathway.Scientific reports · 2025Article
- Interleukin-34 orchestrates bone formation through its binding to bone morphogenic proteins.Theranostics · 2025Article
- Gingival fibroblasts produce paracrine signals that affect osteoclastogenesis in vitro.Bone reports · 2024Article
- Effects of IL-34 and anti-IL-34 neutralizing mAb on alveolar bone loss in a ligature-induced model of periodontitis.Molecular oral microbiology · 2024Article
- Can serum interleukin 34 levels be used as an indicator for the prediction and prognosis of COVID-19?PloS one · 2024Article
- A Lower IL-34 Expression Is Associated with Non-Healing Diabetic Foot Ulcers.Combinatorial chemistry & high throughput screening · 2024Article
- IL-1β and TNF-α play an important role in modulating the risk of periodontitis and Alzheimer's disease.Journal of neuroinflammation · 2023Article
- Molecular Basis beyond Interrelated Bone Resorption/Regeneration in Periodontal Diseases: A Concise Review.International journal of molecular sciences · 2023Review
- Comprehensive single-cell transcriptional profiling defines shared and unique epithelial injury responses during kidney fibrosis.Cell metabolism · 2022Article
- Gingival crevicular fluid CSF-1 and IL-34 levels in patients with stage III grade C periodontitis and uncontrolled type 2 diabetes mellitus.Journal of periodontal & implant science · 2022Article
- Interleukin-34 permits Porphyromonas gingivalis survival and NF-κB p65 inhibition in macrophages.Molecular oral microbiology · 2022Article
- Diagnostic Value of Interleukin-34 as a Novel Biomarker for Severity of Knee Osteoarthritis.Cartilage · 2021Article
- Interleukin-34 promotes tumorigenic signals for colon cancer cells.Cell death discovery · 2021Review
- IL-34 affects fibroblast-like synoviocyte proliferation, apoptosis and function by regulating IL-17.Scientific reports · 2021Article
- Increased Levels of IL-34 in Acquired Immune-Mediated Neuropathies.Journal of molecular neuroscience : MN · 2021Article
- Loss of IL-34 Expression Indicates Poor Prognosis in Patients With Lung Adenocarcinoma.Frontiers in oncology · 2021Article
- The twin cytokines interleukin-34 and CSF-1: masterful conductors of macrophage homeostasis.Theranostics · 2021Review
- Activation of Gingival Fibroblasts by Bacterial Cyclic Dinucleotides and Lipopolysaccharide.Pathogens (Basel, Switzerland) · 2020Article
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2 authors at 2 institutions in 1 country.
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Abstract
backgroundInterleukin-34 (IL-34) is a recently discovered cytokine functionally overlapping macrophage colony stimulating factor (M-CSF), a mediator of inflammation and osteoclastogenesis in bone-degenerative diseases such as rheumatoid arthritis. The objective of this study was to assess the expression of IL-34 in human gingival fibroblasts and investigate if the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α) and Interleukin-1Β (IL-1β) modulate its expression, and moreover if IL-34 could contribute to recruitment of bone-resorbing osteoclasts.
methodsIL-34 expression was evaluated in gingival fibroblasts by real time PCR following stimulation by TNF-α, IL-1β, and treatment with inhibitors of intracellular pathways. The formation of osteoclasts was evaluated by tartrate-resistant acid phosphatase (TRAP) staining of bone marrow macrophages treated with IL-34 or M-CSF in addition to receptor activator of nuclear factor kappa-B ligand (RANKL).
resultsIL-34 was expressed in gingival fibroblasts. The expression was enhanced by TNF-α and IL-1β, regulated by the transcription factor nuclear factor kappa B (NF-κΒ) and activation of c-Jun N-terminal kinase (JNK). Further, IL-34 supports RANKL-induced osteoclastogensis of bone marrow macrophages, independently of M-CSF. SUMMARY: In conclusion, this study shows for the first time IL-34 expression in human gingival fibroblasts, stimulated by TNF-α and IL-1β, key mediators of periodontal inflammation. Furthermore, IL-34 can be substituted for M-CSF in RANKL-induced osteoclastogenesis. IL-34 may contribute to inflammation and osteoclastogenesis in bone-degenerative diseases such as periodontitis.
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