ArticleCell metabolism2015
IL-17A Is Increased in Humans with Primary Hyperparathyroidism and Mediates PTH-Induced Bone Loss in Mice.
Article in Cell metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.
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Who cites it
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- Unravelling the link between chronic inflammation and primary hyperparathyroidism: a systematic review.Frontiers in immunology · 2025Pooled it
- Bacterial specificity of the gut microbiome predicts bone density in primary hyperparathyroidism.Bone research · 2026Article
- Bone metabolism in primary hyperparathyroidism.Wiener klinische Wochenschrift · 2026Review
- C/EBPβ dictates postmenopausal FSHβ transcription and blockade of AEP/C/EBPβ pathway alleviates osteoporosis.Bone research · 2026Article
- Fueling bone loss: the immunometabolic reprogramming of the bone microenvironment in diabetic osteoporosis.Frontiers in immunology · 2026Review
- Myeloid cell expression of the VDR and parathyroid hormone control the host response to influenza infection in mice.Frontiers in immunology · 2026Article
- Intermittent parathyroid hormone (1-34) ameliorates periodontitis via Treg-dependent immunomodulation of the Treg/Th17 axis.Frontiers in immunology · 2026Article
- Circadian rhythms regulate osteoclast recycling through gut microbiota-dependent Th17 cell expansion.Current research in microbial sciences · 2026Article
- Rewiring osteoimmune homeostasis in osteoporosis: T-cell subsets as key regulators and emerging therapeutic targets.Frontiers in immunology · 2026Review
- Hypertension promotes bone loss and fragility by favoring bone resorption in mouse models.The Journal of clinical investigation · 2025Article
- The Alterations in the Osteoimmune Microenvironment of STZ-Induced Type 2 Diabetic Mice:A Single-Cell RNA Sequencing Analysis.Journal of inflammation research · 2025Article
- Associations Among Estrogens, the Gut Microbiome and Osteoporosis.Current osteoporosis reports · 2024Review
- Bone Disease in Primary Hyperparathyroidism-Changes Occurring in Bone Metabolism and New Potential Treatment Strategies.International journal of molecular sciences · 2024Review
- PTHrP participates in the bone destruction of middle ear cholesteatoma via promoting macrophage differentiation into osteoclasts induced by RANKL.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Review
- Osteoimmunology: The Crosstalk between T Cells, B Cells, and Osteoclasts in Rheumatoid Arthritis.International journal of molecular sciences · 2024Review
- Deciphering Immune Landscape Remodeling Unravels the Underlying Mechanism for Synchronized Muscle and Bone Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- An exploration of the causal relationship between 731 immunophenotypes and osteoporosis: a bidirectional Mendelian randomized study.Frontiers in endocrinology · 2024Article
- Inflammation and gut dysbiosis as drivers of CKD-MBD.Nature reviews. Nephrology · 2023Review
- Dietary phosphorus consumption alters T cell populations, cytokine production, and bone volume in mice.JCI insight · 2023Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
Abstract
Primary hyperparathyroidism (PHPT) is a common cause of bone loss that is modeled by continuous PTH (cPTH) infusion. Here we show that the inflammatory cytokine IL-17A is upregulated by PHPT in humans and cPTH in mice. In humans, IL-17A is normalized by parathyroidectomy. In mice, treatment with anti-IL-17A antibody and silencing of IL-17A receptor IL-17RA prevent cPTH-induced osteocytic and osteoblastic RANKL production and bone loss. Mechanistically, cPTH stimulates conventional T cell production of TNFα (TNF), which increases the differentiation of IL-17A-producing Th17 cells via TNF receptor 1 (TNFR1) signaling in CD4(+) cells. Moreover, cPTH enhances the sensitivity of naive CD4(+) cells to TNF via GαS/cAMP/Ca(2+) signaling. Accordingly, conditional deletion of GαS in CD4(+) cells and treatment with the calcium channel blocker diltiazem prevents Th17 cell expansion and blocks cPTH-induced bone loss. Neutralization of IL-17A and calcium channel blockers may thus represent novel therapeutic strategies for hyperparathyroidism.
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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.