ArticleInfection and immunity2009
Involvement of SOCS3 in regulation of CD11c+ dendritic cell-derived osteoclastogenesis and severe alveolar bone loss.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 30 citations in OpenAlex.
- Mechanical licensing of functional dendritic cell states for enhanced T cell priming.bioRxiv : the preprint server for biology · 2026Article
- Developmental Pathways of Immature CD11cInternational journal of molecular sciences · 2026Review
- Conditioned medium from cultured cementoblasts upregulates amelotin gene expression via the SOCS3 signaling pathway.Journal of periodontal & implant science · 2025Article
- Distinct cross talk of IL-17 & TGF-β with the immature CD11cImmunity, inflammation and disease · 2024Article
- Rodent models for oral microbiome research: considerations and challenges- a mini review.Frontiers in oral health · 2024Review
- MiR-218-5p-dependent SOCS3 downregulation increases osteoblast differentiation inpostmenopausal osteoporosis.Journal of orthopaedic surgery and research · 2023Article
- Distinct regulation of myeloid dendritic cell-derived osteoclast precursor (mDDOCp) invokes cytokine milieu-mediated signaling: A new insight into the twist-in-turns of osteoclastogenesis.Journal of dental sciences · 2023Article
- Maintaining homeostatic control of periodontal bone tissue.Periodontology 2000 · 2021Review
- Humanized Mouse Models for the Study of Periodontitis: An Opportunity to Elucidate Unresolved Aspects of Its Immunopathogenesis and Analyze New Immunotherapeutic Strategies.Frontiers in immunology · 2021Review
- Identification of aberrantly expressed long non-coding RNAs in postmenopausal osteoporosis.International journal of molecular medicine · 2018Article
- Overexpression of suppressor of cytokine signaling 3 in dorsal root ganglion attenuates cancer-induced pain in rats.Molecular pain · 2017Article
- SOCS-3 Regulates Alveolar Bone Loss in Experimental Periodontitis.Journal of dental research · 2016Article
- Osteoimmunology and Beyond.Current medicinal chemistry · 2016Review
- Interleukin-2-mediated inhibition of dendritic cell development correlates with decreased CD135 expression and increased monocyte/macrophage precursors.Immunology · 2014Article
- Porphyromonas gingivalis induction of microRNA-203 expression controls suppressor of cytokine signaling 3 in gingival epithelial cells.Infection and immunity · 2011Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
To investigate the role of suppressor of cytokine signaling (SOCS) molecules in periodontal immunity and RANKL-mediated dendritic cell (DC)-associated osteoclastogenesis, we analyzed SOCS expression profiles in CD4(+) T cells and the effect of SOCS3 expression in CD11c(+) DCs during periodontal inflammation-induced osteoclastogenesis and bone loss in nonobese diabetic (NOD) versus humanized NOD/SCID mice. Our results of ex vivo and in vitro analyses showed that (i) there is significantly higher SOCS3 expression associated with RANKL(+) T-cell-mediated bone loss in correlation with increased CD11c(+) DC-mediated osteoclastogenesis; (ii) the transfection of CD11c(+) DC using an adenoviral vector carrying a dominant negative SOCS3 gene significantly abrogates TRAP and bone-resorptive activity; and (iii) inflammation-induced TRAP expression, bone resorption, and SOCS3 activity are not associated with any detectable change in the expression levels of TRAF6 and mitogen-activated protein kinase signaling adaptors (i.e., Erk, Jnk, p38, and Akt) in RANKL(+) T cells. We conclude that SOCS3 plays a critical role in modulating cytokine signaling involved in RANKL-mediated DC-derived osteoclastogenesis during immune interactions with T cells and diabetes-associated severe inflammation-induced alveolar bone loss. Therefore, the development of SOCS3 inhibitors may have therapeutic potential as the target to halt inflammation-induced bone loss under pathological conditions in vivo.
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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.