ArticleThe American journal of pathology2004
Leukocyte-derived interleukin-1beta interacts with renal interleukin-1 receptor I to promote renal tumor necrosis factor and glomerular injury in murine crescentic glomerulonephritis.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 64 citations in OpenAlex.
- Per- and polyfluoroalkyl substances and kidney disease: Genetic associations and computational prioritization of candidate toxicogenomic pathways.PLoS computational biology · 2026Article
- Evaluating Single-Nucleotide Polymorphisms in Inflammasome Proteins and Serum Levels of IL-18 and IL-1β in Kidney Interstitial Damage in Anti-Neutrophilic Cytoplasmic Antibody-Associated Vasculitis.International journal of molecular sciences · 2024Article
- Emerging evidence on the role of clonal hematopoiesis of indeterminate potential in chronic kidney disease.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Glomerulonephritis and autoimmune vasculitis are independent of P2RX7 but may depend on alternative inflammasome pathways.The Journal of pathology · 2022Article
- Review
- ATRvD1 Attenuates Renal Tubulointerstitial Injury Induced by Albumin Overload in Sepsis-Surviving Mice.International journal of molecular sciences · 2021Article
- Molecular Mechanisms Involved in Intrarenal Renin-Angiotensin and Alternative Pathways in Diabetic Nephropathy - A Review.The review of diabetic studies : RDS · 2021Review
- Caspase-1-Inhibitor AC-YVAD-CMK Inhibits Pyroptosis and Ameliorates Acute Kidney Injury in a Model of Sepsis.BioMed research international · 2021Article
- IL-20 in Acute Kidney Injury: Role in Pathogenesis and Potential as a Therapeutic Target.International journal of molecular sciences · 2020Review
- Podocyte Injury Through Interaction BetweenFrontiers in immunology · 2020Article
- Methyl cellosolve-induced renal oxidative stress and time-dependent up-regulation of pro-inflammatory cytokines, apoptotic, and oncogenic markers in rats.Toxicology reports · 2020Article
- Of Inflammasomes and Alarmins: IL-1β and IL-1α in Kidney Disease.Journal of the American Society of Nephrology : JASN · 2016Review
- Protective effects of genetic inhibition of Discoidin Domain Receptor 1 in experimental renal disease.Scientific reports · 2016Article
- Urinary elafin and kidney injury in hematopoietic cell transplant recipients.Clinical journal of the American Society of Nephrology : CJASN · 2015Article
- Proinflammatory Cytokines and Potassium Channels in the Kidney.Mediators of inflammation · 2015Review
- Overexpression of Toll-like receptor 8 correlates with the progression of podocyte injury in murine autoimmune glomerulonephritis.Scientific reports · 2014Article
- Activation of inflammasomes in podocyte injury of mice on the high fat diet: Effects of ASC gene deletion and silencing.Biochimica et biophysica acta · 2014Article
- Interleukin-1β suppresses activity of an inwardly rectifying K+ channel in human renal proximal tubule cells.The journal of physiological sciences : JPS · 2013Article
- Predictive value of conjointly examined IL-1ra, TNF-R I, TNF-R II, and RANTES in patients with primary glomerulonephritis.Journal of Korean medical science · 2013Article
- Distinct contributions of TNF receptor 1 and 2 to TNF-induced glomerular inflammation in mice.PloS one · 2013Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The involvement of proinflammatory cytokines interleukin (IL)-1 and tumor necrosis factor (TNF) in crescentic glomerulonephritis (GN) is well established. Recently the requirement of intrinsic renal cell participation via their production of TNF in crescentic GN was demonstrated. The current studies address the relative contributions of leukocyte and intrinsic renal cell-derived IL-1beta in the induction of TNF production and glomerular injury by studying bone marrow chimeric mice. Leukocyte-derived IL-1beta was critical in the development of crescentic renal injury because IL-1beta(-/-)-->WT (absent leukocyte IL-1beta) chimeric mice had significantly attenuated TNF expression and were protected from the development of crescentic GN. In contrast, WT-->IL-1beta(-/-) chimeric mice (intact leukocyte but absent renal IL-1beta) developed similar TNF expression and crescentic GN to wild-type mice. To determine the cellular target for IL-1 in this model, IL-RI chimeric mice were studied. IL-1RI(-/-)-->WT chimeric (absent leukocyte IL-1RI expression) mice showed no attenuation of crescentic GN, whereas in the absence of renal IL-1RI (WT-->IL-1RI(-/-) chimeras), glomerular TNF expression and the development of crescentic GN were significantly decreased. These studies demonstrate that leukocytes are the major cellular source of IL-1beta, and that IL-1beta acts principally via the IL-1RI on intrinsic renal cells to induce TNF expression and crescentic glomerular injury.
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