ArticleProceedings of the National Academy of Sciences of the United States of America2011
Role of IL-1 receptor-associated kinase-M (IRAK-M) in priming of immune and inflammatory responses by nitrogen bisphosphonates.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Inhibiting METTL3 in macrophages alleviates colitis by enhancing M2 polarization via upregulating IRAKM.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Dysregulation of myddosome complex genes its related to alendronate treatment failure in osteoporosis postmenopausal patients.Genetics and molecular biology · 2026Article
- IL-1 receptor-associated kinase 3 (IRAK3) in lung adenocarcinoma predicts prognosis and immunotherapy resistance: involvement of multiple inflammation-related pathways.Translational lung cancer research · 2024Article
- Modulation of IRAK enzymes as a therapeutic strategy against SARS-CoV-2 induced cytokine storm.Clinical and experimental medicine · 2023Review
- Alendronate reduces periosteal microperfusion in vivo.Heliyon · 2023Article
- Histamine acts via H4-receptor stimulation to cause augmented inflammation when lipopolysaccharide is co-administered with a nitrogen-containing bisphosphonate.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Microcirculatory consequences of limb ischemia/reperfusion in ovariectomized rats treated with zoledronic acid.Journal of orthopaedic surgery and research · 2019Article
- Toll-like receptor 9 expression is associated with breast cancer sensitivity to the growth inhibitory effects of bisphosphonates in vitro and in vivo.Oncotarget · 2016Article
- Mevalonate kinase deficiency leads to decreased prenylation of Rab GTPases.Immunology and cell biology · 2016Article
- Periosteal microcirculatory reactions in a zoledronate-induced osteonecrosis model of the jaw in rats.Clinical oral investigations · 2015Article
- Cytokines as Mediators of Pain-Related Process in Breast Cancer.Mediators of inflammation · 2015Review
- Pulmonary M. tuberculosis infection delays Th1 immunity via immunoadaptor DAP12-regulated IRAK-M and IL-10 expression in antigen-presenting cells.Mucosal immunology · 2014Article
- IL-1 Receptor-Associated Kinase Signaling and Its Role in Inflammation, Cancer Progression, and Therapy Resistance.Frontiers in immunology · 2014Review
- Toll-like receptor mediated regulation of breast cancer: a case of mixed blessings.Frontiers in immunology · 2014Review
- Bisphosphonates target B cells to enhance humoral immune responses.Cell reports · 2013Article
- Zoledronic acid enhances lipopolysaccharide-stimulated proinflammatory reactions through controlled expression of SOCS1 in macrophages.PloS one · 2013Article
- Cutting edge: nitrogen bisphosphonate-induced inflammation is dependent upon mast cells and IL-1.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- The secret ally: immunostimulation by anticancer drugs.Nature reviews. Drug discovery · 2012Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Nitrogen bisphosphonates (NBPs) are commonly prescribed for osteoporosis but have also been found to induce inflammatory reactions and to delay the progression of breast cancer. The inflammatory and anticancer effects of the NBPs might be associated with an ability to modulate innate immune signaling. In mice, intraperitoneal NBP administration causes a rapid influx of neutrophils and monocytes that is dependent on the myeloid differentiation primary response gene 88 (MyD88) mediator of Toll-like receptor (TLR) and IL-1 signaling. Bone marrow chimeras demonstrate that this inflammatory response is partially dependent on TLR4 expression by hematopoietic cells and the IL-1 receptor on radioresistant cells. In vitro, NBPs directly stimulate neither murine bone marrow-derived mononuclear cells nor human peripheral blood mononuclear cells, but rather prime them to produce increased amounts of cytokines when exposed to IL-1 or TLR ligands. This potentiation is mediated by a reduction in IL-1 receptor-associated kinase-M, a negative regulator of MyD88-dependent signaling. In vivo, this property renders the NBPs as effective adjuvants that enhance both cellular and antibody responses to antigens.
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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.