ArticleArthritis & rheumatology (Hoboken, N.J.)2014
CTLA-4Ig-induced T cell anergy promotes Wnt-10b production and bone formation in a mouse model.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 52 citations in OpenAlex.
- Canonical WNT Ligands Produced by Regulatory T Cells Restrain Effector CD4bioRxiv : the preprint server for biology · 2026Article
- Combined Sequential Antiretroviral Therapy-Induced Immune Reconstitution Bone Loss and Estrogen Deficiency Bone Loss Are Cumulative in Mice Models.The Journal of infectious diseases · 2025Article
- Hydroxyurea blunts mitochondrial energy metabolism and osteoblast and osteoclast differentiation exacerbating trabecular bone loss in sickle cell mice.Cell death & disease · 2024Article
- Review
- Wnt10b regulates osteogenesis of adipose-derived stem cells through Wnt/β-catenin signalling pathway in osteoporosis.Cell proliferation · 2024Article
- Changes in bone turnover markers and bone modulators during abatacept treatment.Scientific reports · 2023Observational
- Positive Effects of Biologics on Osteoporosis in Rheumatoid Arthritis.Journal of rheumatic diseases · 2023Review
- The role of WNT10B in physiology and disease: A 10-year update.Frontiers in cell and developmental biology · 2023Review
- Mathematical modeling of the effects of Wnt-10b on bone metabolism.AIChE journal. American Institute of Chemical Engineers · 2022Article
- Immune Reconstitution Bone Loss Exacerbates Bone Degeneration Due to Natural Aging in a Mouse Model.The Journal of infectious diseases · 2022Article
- Mechanisms of joint destruction in rheumatoid arthritis - immune cell-fibroblast-bone interactions.Nature reviews. Rheumatology · 2022Review
- Cyclic Adenosine Monophosphate (cAMP)-Dependent Phosphodiesterase Inhibition Promotes Bone Anabolism Through CD8JBMR plus · 2022Article
- Bone Health in Children with Rheumatic Disorders: Focus on Molecular Mechanisms, Diagnosis, and Management.International journal of molecular sciences · 2022Review
- Effects of Biological/Targeted Therapies on Bone Mineral Density in Inflammatory Arthritis.International journal of molecular sciences · 2022Review
- Article
- Inflammation and Bone Metabolism in Rheumatoid Arthritis: Molecular Mechanisms of Joint Destruction and Pharmacological Treatments.International journal of molecular sciences · 2022Review
- Association between serum bone biomarker levels and therapeutic response to abatacept in patients with rheumatoid arthritis (RA): a multicenter, prospective, and observational RA ultrasound cohort study in Japan.BMC musculoskeletal disorders · 2021Observational
- CTLA-4Ig Improves Hyperalgesia in a Mouse Model of Osteoporosis.International journal of molecular sciences · 2020Article
- Comparative risk of osteoporotic fracture among patients with rheumatoid arthritis receiving TNF inhibitors versus other biologics: a cohort study.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2020Article
- IDO and Kynurenine Metabolites in Peripheral and CNS Disorders.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveRheumatoid arthritis (RA) is an inflammatory autoimmune disease characterized by severe joint erosion and systemic osteoporosis. Chronic T cell activation is a hallmark of RA, and agents that target the CD28 receptor on T cells, which is required for T cell activation, are being increasingly used as therapies for RA and other inflammatory diseases. Lymphocytes play complex roles in the regulation of the skeleton, and although activated T cells and B cells secrete cytokines that promote skeletal decline, under physiologic conditions lymphocytes also have key protective roles in the stabilization of skeletal mass. Consequently, disruption of T cell costimulation may have unforeseen consequences for physiologic bone turnover. This study was undertaken to investigate the impact of pharmacologic CD28 T cell costimulation blockade on physiologic bone turnover and structure.
methodsC57BL6 mice were treated with CTLA-4Ig, a pharmacologic CD28 antagonist or with irrelevant control antibody (Ig), and serum biochemical markers of bone turnover were quantified by enzyme-linked immunosorbent assay. Bone mineral density and indices of bone structure were further measured by dual x-ray absorptiometry and micro-computed tomography, respectively, and static and dynamic indices of bone formation were quantified using bone histomorphometry.
resultsPharmacologic disruption of CD28 T cell costimulation in mice significantly increased bone mass and enhanced indices of bone structure, a consequence of enhanced bone formation, concurrent with enhanced secretion of the bone anabolic factor Wnt-10b by T cells.
conclusionInhibition of CD28 costimulation by CTLA-4Ig promotes T cell Wnt-10b production and bone formation and may represent a novel anabolic strategy for increasing bone mass in osteoporotic conditions.
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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.