ArticleBiochemical and biophysical research communications2014
Potential role of myeloid cell/eosinophil-derived IL-17 in LPS-induced endotoxin shock.
Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Interleukin-6 related signaling pathways as the intersection between chronic diseases and sepsis.Molecular medicine (Cambridge, Mass.) · 2025Review
- The dual role of IL-17 in periodontitis regulating immunity and bone homeostasis.Frontiers in immunology · 2025Review
- IL-17 and IL-21: Their Immunobiology and Therapeutic Potentials.Immune network · 2024Review
- Article
- Ultra-endurance triathlon performance and markers of whole-body and gut-specific inflammation.European journal of applied physiology · 2020Article
- Biology of Interleukin-17 and Its Pathophysiological Significance in Sepsis.Frontiers in immunology · 2020Review
- Innate Cells: The Alternative Source of IL-17 in Axial and Peripheral Spondyloarthritis?Frontiers in immunology · 2020Review
- A Novel Chinese Medicine, Xinfeng Capsule, Modulates Proinflammatory Cytokines via Regulating the Toll-Like Receptor 4 (TLR4)/Mitogen-Activated Protein Kinase (MAPK)/Nuclear Kappa B (NF-κB) Signaling Pathway in an Adjuvant Arthritis Rat Model.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- The roles of IL-17C in T cell-dependent and -independent inflammatory diseases.Scientific reports · 2018Article
- Central Role of IL-23 and IL-17 Producing Eosinophils as Immunomodulatory Effector Cells in Acute Pulmonary Aspergillosis and Allergic Asthma.PLoS pathogens · 2017Article
- Vasoactive intestinal peptide suppresses macrophage-mediated inflammation by downregulating interleukin-17A expression via PKA- and PKC-dependent pathways.International journal of experimental pathology · 2015Article
Corrections and comments
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Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
Abstract
IL-17RA is a shared receptor subunit for several cytokines of the IL-17 family, including IL-17A, IL-17C, IL-17E (also called IL-25) and IL-17F. It has been shown that mice deficient in IL-17RA are more susceptible to sepsis than wild-type mice, suggesting that IL-17RA is important for host defense against sepsis. However, it is unclear which ligands for IL-17RA, such as IL-17A, IL-17C, IL-17E/IL-25 and/or IL-17F, are involved in the pathogenesis of sepsis. Therefore, we examined IL-17A, IL-17E/IL-25 and IL-17F for possible involvement in LPS-induced endotoxin shock. IL-17A-deficient mice, but not IL-25- or IL-17F-deficient mice, were resistant to LPS-induced endotoxin shock, as compared with wild-type mice. Nevertheless, studies using IL-6-deficient, IL-21Rα-deficient and Rag-2-deficient mice, revealed that neither IL-6 and IL-21, both of which are important for Th17 cell differentiation, nor Th17 cells were essential for the development of LPS-induced endotoxin shock, suggesting that IL-17A-producing cells other than Th17 cells were important in the setting. In this connection, IL-17A was produced by macrophages, DCs and eosinophils after LPS injection. Taken together, these findings indicate that IL-17A, but not IL-17F or IL-25, is crucial for LPS-induced endotoxin shock. In addition, macrophages, DCs and eosinophils, but not Th17 cells or γδ T cells, may be sources of IL-17A during LPS-induced endotoxin shock.
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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.