ArticleBoneKEy reports2012
Cross-talk between T cells and osteoclasts in bone resorption.
Article in BoneKEy reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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
26 citing papers in PubMed, 44 citations in OpenAlex.
- Breaking down to rebuild: lymphatic ablation enhances osteoclast-driven regeneration.The Journal of clinical investigation · 2026Article
- T cell related osteoimmunology in fracture healing: Potential targets for augmenting bone regeneration.Journal of orthopaedic translation · 2025Review
- Cinchonine: A Versatile Pharmacological Agent Derived from Natural Cinchona Alkaloids.Current topics in medicinal chemistry · 2024Review
- Advanced 3D Magnetic Scaffolds for Tumor-Related Bone Defects.International journal of molecular sciences · 2022Review
- Topography-mediated immunomodulation in osseointegration; Ally or Enemy.Biomaterials · 2022Review
- LIM Homeobox Transcription Factor 1-β Expression is Upregulated in Patients with Osteolysis after Total Ankle Arthroplasty and Inhibits Receptor Activator of Nuclear Factor-κB Ligand-Induced Osteoclast Differentiation in Vitro.Journal of bone metabolism · 2022Article
- The Role of TAK1 in RANKL-Induced Osteoclastogenesis.Calcified tissue international · 2022Review
- mTOR Signaling in the Regulation of CD4+ T Cell Subsets in Periodontal Diseases.Frontiers in immunology · 2022Review
- IL4/IL4R signaling promotes the osteolysis in metastatic bone of CRC through regulating the proliferation of osteoclast precursors.Molecular medicine (Cambridge, Mass.) · 2021Article
- Control of innate immune response by biomaterial surface topography, energy, and stiffness.Acta biomaterialia · 2021Review
- Celastrol Attenuates RANKL-Induced OsteoclastogenesisFrontiers in pharmacology · 2021Article
- Network-based Transcriptome-wide Expression Study for Postmenopausal Osteoporosis.The Journal of clinical endocrinology and metabolism · 2020Article
- C reactive protein impairs adaptive immunity in immune cells of patients with melanoma.Journal for immunotherapy of cancer · 2020Article
- Microtopography of Immune Cells in Osteoporosis and Bone Lesions by Endocrine Disruptors.Frontiers in immunology · 2020Review
- Transcriptional Regulation of Osteoclastogenesis: The Emerging Role of KLF2.Frontiers in immunology · 2020Review
- What Are the Peripheral Blood Determinants for Increased Osteoclast Formation in the Various Inflammatory Diseases Associated With Bone Loss?Frontiers in immunology · 2019Review
- Multiple Myeloma and Bone: The Fatal Interaction.Cold Spring Harbor perspectives in medicine · 2018Review
- Lamins and bone disorders: current understanding and perspectives.Oncotarget · 2018Review
- Role of Marrow Adipocytes in Regulation of Energy Metabolism and Bone Homeostasis.Current osteoporosis reports · 2018Review
- Functional Activation of Osteoclast Commitment in Chronic Lymphocytic Leukaemia: a Possible Role for RANK/RANKL Pathway.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoclasts (OCs) are the exclusive bone resorptive cell, they derive from monocyte/macrophage precursors, which can circulate within the hematopoietic cell pool or be resident in a number of tissues. The maintenance of an adequate bone mass depends on the controlled and timely removal of old, damaged bone. The increase of OC activity is observed in many pathologies characterised by bone loss, such as osteoporosis, rheumatoid arthritis, bone metastasis, periprosthetic osteolysis in aseptic loosening of arthroplasty and also in pediatric diseases, such as phenilketonuria and 21-hydroxylase deficiency. During the bone resorption process there is an intense cross-talk between immune system cells and OCs. In particular, T cells release factors and cytokines, which rule osteoclastogenesis, and on the other hand, OCs produce factors that act on T cells. A primary mediator of osteoclastogenesis is the receptor activator of nuclear factor-κβ-RANK ligand-osteoprotegerin system, but also other cytokines promote OC activation according to the different pathologies. This review summarizes the main mechanisms promoting osteoclastogenesis in diseases characterised by bone loss, focusing on factors and cytokines involved in this process and on the interaction between OCs and T cells.
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.