ArticleJCI insight2021
RTEC-intrinsic IL-17-driven inflammatory circuit amplifies antibody-induced glomerulonephritis and is constrained by Regnase-1.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- The regnase family in autoimmune diseases: a regnase-1-centered perspective on cellular heterogeneity.Molecular biology reports · 2026Review
- The RNA binding protein Arid5a is an activator of TNF signaling in rheumatoid arthritis.JCI insight · 2026Article
- C/EBPδ Mediates Immunity to Renal Autoinflammatory Disorders in a Stage-specific Manner.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Pancreatic Epithelial IL17/IL17RA Signaling Drives B7-H4 Expression to Promote Tumorigenesis.Cancer immunology research · 2024Article
- The RNA binding protein Arid5a drives IL-17-dependent autoantibody-induced glomerulonephritis.The Journal of experimental medicine · 2024Article
- Differential Expression of Anti-Inflammatory RNA Binding Proteins in Lupus Nephritis.Life (Basel, Switzerland) · 2022Article
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Antibody-mediated glomerulonephritis (AGN) is a clinical manifestation of many autoimmune kidney diseases for which few effective treatments exist. Chronic inflammatory circuits in renal glomerular and tubular cells lead to tissue damage in AGN. These cells are targeted by the cytokine IL-17, which has recently been shown to be a central driver of the pathogenesis of AGN. However, surprisingly little is known about the regulation of pathogenic IL-17 signaling in the kidney. Here, using a well-characterized mouse model of AGN, we show that IL-17 signaling in renal tubular epithelial cells (RTECs) is necessary for AGN development. We also show that Regnase-1, an RNA binding protein with endoribonuclease activity, is a negative regulator of IL-17 signaling in RTECs. Accordingly, mice with a selective Regnase-1 deficiency in RTECs exhibited exacerbated kidney dysfunction in AGN. Mechanistically, Regnase-1 inhibits IL-17-driven expression of the transcription factor IκBξ and, consequently, its downstream gene targets, including Il6 and Lcn2. Moreover, deletion of Regnase-1 in human RTECs reduced inflammatory gene expression in a IκBξ-dependent manner. Overall, these data identify an IL-17-driven inflammatory circuit in RTECs during AGN that is constrained by Regnase-1.
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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.