ArticleAnnals of the New York Academy of Sciences2010
Inhibition of antigen presentation and T cell costimulation blocks PTH-induced bone loss.
Article in Annals of the New York Academy of Sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Low baseline CD4+ count is associated with greater bone mineral density loss after antiretroviral therapy initiation.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2013Trial
- The role of microscopic properties on cortical bone strength of femoral neck.BMC musculoskeletal disorders · 2023Article
- Positive Effects of Biologics on Osteoporosis in Rheumatoid Arthritis.Journal of rheumatic diseases · 2023Review
- The Effect of Anti-rheumatic Drugs on the Skeleton.Calcified tissue international · 2022Review
- Cyclic Adenosine Monophosphate (cAMP)-Dependent Phosphodiesterase Inhibition Promotes Bone Anabolism Through CD8JBMR plus · 2022Article
- Beyond Bone: Infectious Diseases and Immunity in Parathyroid Disorders.Advances in experimental medicine and biology · 2022Article
- Modulation of Macrophage Activity by Pulsed Electromagnetic Fields in the Context of Fracture Healing.Bioengineering (Basel, Switzerland) · 2021Article
- Comparative risk of malignancies and infections in patients with rheumatoid arthritis initiating abatacept versus other biologics: a multi-database real-world study.Arthritis research & therapy · 2019Observational
- Abaloparatide exhibits greater osteoanabolic response and higher cAMP stimulation and β-arrestin recruitment than teriparatide.Physiological reports · 2019Article
- CTLA-4Ig (abatacept) balances bone anabolic effects of T cells and Wnt-10b with antianabolic effects of osteoblastic sclerostin.Annals of the New York Academy of Sciences · 2018Article
- Bone and the Immune System.Toxicologic pathology · 2017Review
- Parathyroid Diseases and T Cells.Current osteoporosis reports · 2017Review
- Absence of miR-182 Augments Cardiac Allograft Survival.Transplantation · 2017Article
- Biologic therapies and bone loss in rheumatoid arthritis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2017Review
- Physiological and pathophysiological bone turnover - role of the immune system.Nature reviews. Endocrinology · 2016Review
- Bone-immune cell crosstalk: bone diseases.Journal of immunology research · 2015Review
- T-cells and B-cells in osteoporosis.Current opinion in endocrinology, diabetes, and obesity · 2014Review
- CTLA-4Ig-induced T cell anergy promotes Wnt-10b production and bone formation in a mouse model.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Bone remodelling markers in rheumatoid arthritis.Mediators of inflammation · 2014Review
- Role of T cells in the modulation of PTH action: physiological and clinical significance.Endocrine · 2013Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
T cells are required for continuous parathyroid hormone (cPTH) treatment to induce bone loss as they sensitize stromal cells to PTH through CD40 ligand (CD40L), a surface molecule of activated T cells. Since CD40L expression is a feature of activated T cells, we investigated whether antigen (Ag)-mediated T cell activation is required for PTH to exert its catabolic activity. We report that inhibition of Ag presentation through silencing of either class I or class II MHC-T cell receptor (TCR) interaction prevents the cortical bone loss induced by in vivo cPTH treatment. We also show that the bone loss and the stimulation of bone resorption induced by cPTH treatment are prevented by CTLA4-Ig, an inhibitor of T cell costimulation approved for the treatment of rheumatoid arthritis. Since inhibition of antigen-driven T cell activation by blockade of either TCR signaling or T cell costimulation is sufficient to silence the catabolic activity of cPTH, antigen-presenting cells and T lymphocyte interactions therefore play a critical role in the mechanism of action of PTH.
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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.