ArticleThe American journal of pathology2011
Interleukin-17A promotes early but attenuates established disease in crescentic glomerulonephritis in mice.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- Systemic Implications of Bullous Pemphigoid: Bridging Dermatology and Internal Medicine.Diagnostics (Basel, Switzerland) · 2024Review
- Review
- Urinary T Cells Identify Renal Antineutrophil Cytoplasmic Antibody-Associated Vasculitis and Predict Prognosis: A Proof of Concept Study.Kidney international reports · 2023Article
- The Development of Systemic Inflammatory Diseases in Hidradenitis Suppurativa.Diagnostics (Basel, Switzerland) · 2023Review
- Differentiation of crescent-forming kidney progenitor cells into podocytes attenuates severe glomerulonephritis in mice.Science translational medicine · 2022Article
- Review
- Psoriasis and Systemic Inflammatory Disorders.International journal of molecular sciences · 2022Review
- The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation.International journal of molecular sciences · 2021Review
- Immune regulation in renal inflammation.Cell and tissue research · 2021Review
- ANCA-Associated Vasculitis: An Update.Journal of clinical medicine · 2021Review
- Crescentic Glomerulonephritis: Pathogenesis and Therapeutic Potential of Human Amniotic Stem Cells.Frontiers in physiology · 2021Review
- Growth Differentiation Factor 15 Ameliorates Anti-Glomerular Basement Membrane Glomerulonephritis in Mice.International journal of molecular sciences · 2020Article
- Transient Expression of IL-17A in Foxp3 Fate-Tracked Cells inFrontiers in immunology · 2020Article
- Interleukin 17A promotes diabetic kidney injury.Scientific reports · 2019Article
- IL-12 and IL-23/Th17 axis in systemic lupus erythematosus.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- IL-17 in Renal Immunity and Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2018Review
- A model of TH17-associated ileal hyperplasia that requires both IL-17A and IFNγ to generate self-tolerance and prevent colitis.Mucosal immunology · 2018Article
- Article
- Chemokine receptor co-expression reveals aberrantly distributed TArthritis research & therapy · 2017Article
- Milk fat globule-EGF factor 8 suppresses the aberrant immune response of systemic lupus erythematosus-derived neutrophils and associated tissue damage.Cell death and differentiation · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T helper (Th)17 cells might contribute to immune-mediated renal injury. Thus, we sought to define the time course of IL-17A-induced kidney damage and examined the relation between Th17 and Th1 cells in a model of crescentic anti-glomerular basement membrane glomerulonephritis. Renal injury and immune responses were assessed in wild-type and in IL-17A-deficient mice on days 6, 14, and 21 of disease development. On day 6, when mild glomerulonephritis developed, IL-17A-deficient mice were protected from renal injury. On day 14, when more severe disease developed, protection from renal injury due to IL-17A deficiency was less evident. On day 21, when crescentic glomerulonephritis was fully established, disease was enhanced in IL-17A(-/-) mice, with increased glomerular T-cell accumulation and fibrin deposition, and augmented Th1 responses. Mice lacking the Th17-promoting cytokine, IL-23 (p19), also developed more severe disease than wild-type animals on day 21. In contrast, mice deficient in the key Th1-promoting cytokine, IL-12 (p35), had decreased Th1 and increased Th17 responses and developed less severe crescentic glomerulonephritis than wild-type animals. These studies show that IL-17A contributes to early glomerular injury, but it attenuates established crescentic glomerulonephritis by suppressing Th1 responses. They provide further evidence that Th1 cells mediate crescentic injury in this model and that Th1 and Th17 cells counterregulate each other during disease development.
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