ArticleThe Journal of biological chemistry2017
Interleukin 27 (IL-27) Alleviates Bone Loss in Estrogen-deficient Conditions by Induction of Early Growth Response-2 Gene.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Role of Cytokines in Bone Diseases and Their Therapeutic Application.ImmunoTargets and therapy · 2026Review
- Unraveling the causal role of TGF-βRII in osteoporosis and the potential of its associated differential genes as novel targets.European journal of medical research · 2025Article
- Identification of osteoarthritis-associated chondrocyte subpopulations and key gene-regulating drugs based on multi-omics analysis.Scientific reports · 2025Article
- Multi-omics Analysis to Identify Key Immune Genes for Osteoporosis based on Machine Learning and Single-cell Analysis.Orthopaedic surgery · 2024Article
- Divergent associations of inflammatory markers with bone turnover markers in elderly patients with osteoporotic fractures.Scientific reports · 2024Article
- Causal relationship between Interleukin-27 expression levels and osteoporosis: a bidirectional mendelian randomization study.BMC musculoskeletal disorders · 2024Article
- Exploring the Role of Hormones and Cytokines in Osteoporosis Development.Biomedicines · 2024Review
- Targeting bone homeostasis regulation: potential of traditional Chinese medicine flavonoids in the treatment of osteoporosis.Frontiers in pharmacology · 2024Review
- L-BAIBA Synergizes with Sub-Optimal Mechanical Loading to Promote New Bone Formation.JBMR plus · 2023Article
- Molecular Basis beyond Interrelated Bone Resorption/Regeneration in Periodontal Diseases: A Concise Review.International journal of molecular sciences · 2023Review
- The role of retinoic acid receptor-related orphan receptors in skeletal diseases.Frontiers in endocrinology · 2023Review
- Mechanism of regulating macrophages/osteoclasts in attenuating wear particle-induced aseptic osteolysis.Frontiers in immunology · 2023Review
- The effect of cytokines on osteoblasts and osteoclasts in bone remodeling in osteoporosis: a review.Frontiers in immunology · 2023Review
- Review
- Morphological and Mechanical Characterization of Extracellular Vesicles and Parent Human Synoviocytes under Physiological and Inflammatory Conditions.International journal of molecular sciences · 2022Article
- Systemic IL-27 administration prevents abscess formation and osteolysis via local neutrophil recruitment and activation.Bone research · 2022Article
- Stimulation of Osteoclast Formation by Oncostatin M and the Role of WNT16 as a Negative Feedback Regulator.International journal of molecular sciences · 2022Review
- Interplay between Inflammation and Pathological Bone Resorption: Insights into Recent Mechanisms and Pathways in Related Diseases for Future Perspectives.International journal of molecular sciences · 2022Review
- Prognostic analysis and validation of diagnostic marker genes in patients with osteoporosis.Frontiers in immunology · 2022Article
- MiR-539-3p impairs osteogenesis by suppressing Wnt interaction with LRP-6 co-receptor and subsequent inhibition of Akap-3 signaling pathway.Frontiers in endocrinology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A growing understanding of the bone remodeling process suggests that inflammation significantly contributes to the pathogenesis of osteoporosis. T cells and various cytokines contribute majorly to the estrogen deficiency-induced bone loss. Recent studies have identified the IL-12 cytokine family as consisting of pro-inflammatory IL-12 and IL-23 and the anti-inflammatory IL-27 and IL-35 cytokines. IL-27 exerts protective effects in autoimmune diseases like experimental autoimmune encephalomyelitis; however, its role in the pathogenesis of osteoporosis remains to be determined. In this report, we study the effect of IL-27 supplementation on ovariectomized estrogen-deficient mice on various immune and skeletal parameters. IL-27 treatment in ovariectomized mice suppressed Th17 cell differentiation by inhibiting transcription factor RORγt. Supplementation of IL-27 activates Egr-2 to induce IL-10 producing Tr1 cells. IL-27 treatment prevented the loss of trabecular micro-architecture and preserved cortical bone parameters. IL-27 also inhibited osteoblast apoptosis through increased Egr-2 expression, which induces anti-apoptotic factors like MCL-1. IL-27 suppressed osteoclastogenesis in an Egr-2-dependent manner that up-regulates Id2, the repressor of the receptor activator of nuclear factor-κB ligand-mediated osteoclastogenesis. Additionally, these results were corroborated in female osteoporotic subjects where we found decreased serum IL-27 levels along with reduced Egr-2 expression. Our study forms a strong basis for using humanized IL-27 toward the treatment of post-menopausal osteoporosis.
Indexed as
Identifiers
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.