ArticleMediators of inflammation2014
TLR2 elicits IL-17-mediated RANKL expression, IL-17, and OPG production in neutrophils from arthritic mice.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- The mode of action of IL-23 in experimental inflammatory arthritic pain and disease.Arthritis research & therapy · 2024Article
- Pathological progression of osteoarthritis: a perspective on subchondral bone.Frontiers of medicine · 2024Review
- Upregulation of osteoprotegerin inhibitsExperimental and therapeutic medicine · 2022Article
- Serum osteoprotegerin level in hemodialysis patients using low-flux reused dialyzer in relation to atherosclerosis.Journal of clinical laboratory analysis · 2021Article
- Cigarette Smoke-Induced Lymphoid Neogenesis in COPD Involves IL-17/RANKL Pathway.Frontiers in immunology · 2020Article
- IL-17 PromotesJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Interleukin-17A Deficiency Attenuated Emphysema and Bone Loss in Mice Exposed to Cigarette Smoke.International journal of chronic obstructive pulmonary disease · 2020Article
- Role of Chemokines and Chemokine Receptors in Rheumatoid Arthritis.ImmunoTargets and therapy · 2020Review
- Immunopathogenic Mechanisms and Novel Immune-Modulated Therapies in Rheumatoid Arthritis.International journal of molecular sciences · 2019Review
- The Role of Osteoprotegerin and Its Ligands in Vascular Function.International journal of molecular sciences · 2019Review
- Characterization and biological significance of IL-23-induced neutrophil polarization.Cellular & molecular immunology · 2018Article
- Role of toll-like receptor 2 in inflammation and alveolar bone loss in experimental peri-implantitis versus periodontitis.Journal of periodontal research · 2018Article
- Immune modulation of some autoimmune diseases: the critical role of macrophages and neutrophils in the innate and adaptive immunity.Journal of translational medicine · 2017Review
- A pathogenic IFNα, BLyS and IL-17 axis in Systemic Lupus Erythematosus patients.Scientific reports · 2016Article
- Neutrophils Do Not Express IL-17A in the Context of Acute Oropharyngeal Candidiasis.Pathogens (Basel, Switzerland) · 2015Article
- The effect of interleukin 17 and Toll-like receptor 2 on CD11b expression and apoptosis of neutrophils in zymosaninduced arthritis and paw oedema.Central-European journal of immunology · 2014Article
- Overexpression of hepatic serum amyloid A1 in mice increases IL-17-producing innate immune cells and decreases bone density.The Journal of biological chemistryArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the ability of neutrophils to express receptor activator of nuclear factor kappa-B ligand (RANKL), to secrete osteoprotegerin (OPG), and to produce IL-17. Arthritis was induced by intra-articular injection of zymosan, a ligand for Toll-like receptor 2 (TLR2). Frequencies of neutrophils in bone marrow (BM), blood and synovial fluid (SF), receptor expression, and cytokine production were evaluated by flow cytometry. 1A8 antibody (1A8 Ab) was used to deplete neutrophils in zymosan-injected SCID mice. IL-17, RANKL, and OPG amounts in SF, serum, or cell cultures were determined by ELISA. The development of arthritis was associated with increased secretion of IL-17, RANKL, and OPG in serum and SF, elevated frequencies of Ly6G(+)CD11b(+) cells in BM, blood, and SF and upregulated RANKL expression. Both IL-17 and OPG were absent in serum and SF after neutrophil depletion; therefore we assume that they were released by neutrophils. In vitro blood Ly6G(+)CD11b(+) cells from arthritic mice produced spontaneously IL-17, IFN-γ, and OPG and expressed RANKL. This phenotype was sustained by IL-17. TLR2 engagement increased IL-17 and IFN-γ production, potentiated IL-17-mediated RANKL expression, and inhibited OPG secretion. We conclude that TLR2 regulates the destructive potential of neutrophils and its targeting might limit joint alterations in arthritis.
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