ArticleClinical immunology (Orlando, Fla.)2009
Oxidized lipids enhance RANKL production by T lymphocytes: implications for lipid-induced bone loss.
Article in Clinical immunology (Orlando, Fla.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 95 citations in OpenAlex.
- Specific serotonin receptor antagonist reduces murine calcific atherosclerosis.Atherosclerosis · 2026Article
- The impact of dyslipidemia on skeletal health - from an immunoregulatory perspective.Frontiers in immunology · 2026Review
- β-Catenin: A Key Molecule in Osteoblast Differentiation.Biomolecules · 2025Review
- Obesity and lipid metabolism in the development of osteoporosis (Review).International journal of molecular medicine · 2024Review
- Unraveling ferroptosis in osteogenic lineages: implications for dysregulated bone remodeling during periodontitis progression.Cell death discovery · 2024Article
- Association of Decreased Bone Density and Hyperlipidemia in a Taiwanese Older Adult Population.Journal of the Endocrine Society · 2024Article
- Kefir peptides attenuate atherosclerotic vascular calcification and osteoporosis in atherogenic diet-fedFrontiers in cell and developmental biology · 2023Article
- ApoA-I mimetics reduce systemic and gut inflammation in chronic treated HIV.PLoS pathogens · 2022Article
- Neutralization of oxidized phospholipids attenuates age-associated bone loss in mice.Aging cell · 2021Article
- Association of dyslipidaemia with osteoporosis in postmenopausal women.The Journal of international medical research · 2021Article
- A Neutralizing Antibody Targeting Oxidized Phospholipids Promotes Bone Anabolism in Chow-Fed Young Adult Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- RANKL Expression Is Increased in Circulating Mononuclear Cells of Patients with Calcific Aortic Stenosis.Journal of cardiovascular translational research · 2018Article
- Oxidation-specific epitopes restrain bone formation.Nature communications · 2018Article
- Lipoproteins in Cardiovascular Calcification: Potential Targets and Challenges.Frontiers in cardiovascular medicine · 2018Review
- Human immune compartment comparisons: Optimization of proliferative assays for blood and gut T lymphocytes.Journal of immunological methods · 2017Article
- Distinct aging profiles of CD8+ T cells in blood versus gastrointestinal mucosal compartments.PloS one · 2017Article
- Oxidized lipoproteins are associated with markers of inflammation and immune activation in HIV-1 infection.AIDS (London, England) · 2016Article
- The silent war of CMV in aging and HIV infection.Mechanisms of ageing and development · 2016Review
- Dyslipidemia and Diabetes Increase the OPG/TRAIL Ratio in the Cardiovascular System.Mediators of inflammation · 2016Article
- Bone Loss Triggered by the Cytokine Network in Inflammatory Autoimmune Diseases.Journal of immunology research · 2015Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Osteoporosis is a systemic disease that is associated with increased morbidity, mortality and health care costs. Whereas osteoclasts and osteoblasts are the main regulators of bone homeostasis, recent studies underscore a key role for the immune system, particularly via activation-induced T lymphocyte production of receptor activator of NFkappaB ligand (RANKL). Well-documented as a mediator of T lymphocyte/dendritic cell interactions, RANKL also stimulates the maturation and activation of bone-resorbing osteoclasts. Given that lipid oxidation products mediate inflammatory and metabolic disorders such as osteoporosis and atherosclerosis, and since oxidized lipids affect several T lymphocyte functions, we hypothesized that RANKL production might also be subject to modulation by oxidized lipids. Here, we show that short term exposure of both unstimulated and activated human T lymphocytes to minimally oxidized low density lipoprotein (LDL), but not native LDL, significantly enhances RANKL production and promotes expression of the lectin-like oxidized LDL receptor-1 (LOX-1). The effect, which is also observed with 8-iso-Prostaglandin E2, an inflammatory isoprostane produced by lipid peroxidation, is mediated via the NFkappaB pathway, and involves increased RANKL mRNA expression. The link between oxidized lipids and T lymphocytes is further reinforced by analysis of hyperlipidemic mice, in which bone loss is associated with increased RANKL mRNA in T lymphocytes and elevated RANKL serum levels. Our results suggest a novel pathway by which T lymphocytes contribute to bone changes, namely, via oxidized lipid enhancement of RANKL production. These findings may help elucidate clinical associations between cardiovascular disease and decreased bone mass, and may also lead to new immune-based approaches to osteoporosis.
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Registered trials
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