ReviewFrontiers in immunology2019
Finding a Toll on the Route: The Fate of Osteoclast Progenitors After Toll-Like Receptor Activation.
Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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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
43 citing papers in PubMed, 68 citations in OpenAlex.
- Microbial messengers: decoding the gut microbiota's role in bone health through immunomodulation and exosomal signaling.NPJ biofilms and microbiomes · 2026Review
- Systemic cachexia and muscle-bone crosstalk drive depression-related joint remodeling and pain.International journal of surgery (London, England) · 2026Article
- Hyperbaric oxygen protects against periodontal bone loss by modulating inflammation and bone remodeling via RANKL/OPG expression in ligature-induced periodontitis.International journal of medical sciences · 2026Article
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- Article
- Reduced Bone Quality of Sacrum and Lumbal Vertebrae Spongiosa in Toll-like Receptor 2- and Toll-like Receptor 4-Knockout Mice: A Blinded Micro-Computerized Analysis.Biomolecules · 2025Article
- Osteoclast Activation and Inflammatory Bone Diseases: Focusing on Receptors in Osteoclasts.Journal of inflammation research · 2025Review
- Osteogenic CpG Oligodeoxynucleotide, iSN40, Inhibits Osteoclastogenesis in a TLR9-Dependent Manner.Life (Basel, Switzerland) · 2024Article
- PTEN: an emerging target in rheumatoid arthritis?Cell communication and signaling : CCS · 2024Review
- Vertebral destruction in tuberculous spondylitis correlates with Toll-like Receptor 4 (TLR-4) levels: a cross-sectional study.Annals of medicine and surgery (2012) · 2024Article
- Infrapatellar fat pad adipose tissue-derived macrophages display a predominant CD11c+CD206+ phenotype and express genotypes attributable to key features of OA pathogenesis.Frontiers in immunology · 2024Article
- The role of innate immunity in diabetic nephropathy and their therapeutic consequences.Journal of pharmaceutical analysis · 2024Review
- Staphylococci planktonic and biofilm environments differentially affect osteoclast formation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Inhibition of Toll-Like Receptor 4 Signaling Pathway Accelerates the Repair of Avascular Necrosis of Femoral Epiphysis through Regulating Macrophage Polarization in Perthes Disease.Tissue engineering and regenerative medicine · 2023Article
- RANKeLife · 2023Article
- Targeting strategies for bone diseases: signaling pathways and clinical studies.Signal transduction and targeted therapy · 2023Review
- Toll-like receptor 4 signaling in osteoblasts is required for load-induced bone formation in mice.iScience · 2023Article
- Article
- TLR9 Mediates Periodontal Aging by Fostering Senescence and Inflammaging.Journal of dental research · 2022Article
- Topography-mediated immunomodulation in osseointegration; Ally or Enemy.Biomaterials · 2022Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
M-CSF and RANKL are two crucial cytokines stimulating differentiation of mature, bone resorbing, multinucleated osteoclasts from mononucleated progenitor cells in the monocyte/macrophage lineage. In addition to the receptors for M-CSF and RANKL, osteoclast progenitor cells express receptors for several other pro- and anti-osteoclastogenic cytokines, which also regulate osteoclast formation by affecting signaling downstream M-CSF and RANKL receptors. Similar to many other cells originating from myeloid hematopoetic stem cells, also osteoclast progenitors express toll-like receptors (TLRs). Nine murine TLRs are expressed in the progenitors and all, with the exception of TLR2 and TLR4, are downregulated during osteoclastogenesis. Activation of TLR2, TLR4, and TLR9, but not TLR5, in osteoclast progenitors stimulated with M-CSF and RANKL arrests differentiation along the osteoclastic lineage and keeps the cells at a macrophage stage. When the progenitors are primed with M-CSF/RANKL and then stimulated with agonists for TLR2, TLR4, or TLR9 in the presence of M-CSF, but in the absence of RANKL, the cells differentiate to mature, bone resorbing osteoclasts. TLR 2, 4, 5, and 9 are also expressed on osteoblasts and their activation increases osteoclast differentiation by an indirect mechanism through stimulation of RANKL. In mice, treatment with agonists for TLR2, 4, and 5 results in osteoclast formation and extensive bone loss. It remains to be shown the relative importance of inhibitory and stimulatory effects by TLRs on osteoclast progenitors and the role of RANKL produced by TLR stimulated osteoblasts, for the bone resorbing effects
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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.