ArticleClinical and experimental immunology2014
Endogenous interleukin (IL)-17A promotes pristane-induced systemic autoimmunity and lupus nephritis induced by pristane.
Article in Clinical and experimental immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 45 citations in OpenAlex.
- Enhancing the treatment potential of IL-17 antagonism in lupus nephritis: finding the right partner.Frontiers in immunology · 2025Review
- DNA Nanoflowers' Amelioration of Lupus Symptoms in Mice via Blockade of TLR7/9's Signal.International journal of molecular sciences · 2022Article
- Effects of Astragalus membranaceus on systemic lupus erythematosus in a mouse model of pregnancy.Immunity, inflammation and disease · 2022Review
- A Mechanistic Insight into the Pathogenic Role of Interleukin 17A in Systemic Autoimmune Diseases.Mediators of inflammation · 2022Review
- The role of Treg subtypes in glomerulonephritis.Cell and tissue research · 2021Review
- Contribution of Th17 cells to tissue injury in hypertension.Current opinion in nephrology and hypertension · 2021Review
- T helper 17 cells in the pathophysiology of acute and chronic kidney disease.Kidney research and clinical practice · 2021Article
- Hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus.Physiological reports · 2021Article
- The Th17/IL-17 Axis and Kidney Diseases, With Focus on Lupus Nephritis.Frontiers in medicine · 2021Review
- Tertiary lymphoid organs are associated with the progression of kidney damage and regulated by interleukin-17A.Theranostics · 2021Article
- Regulation of the germinal center response by nuclear receptors and implications for autoimmune diseases.The FEBS journal · 2020Review
- IL-12 and IL-23/Th17 axis in systemic lupus erythematosus.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Environmental Exposures and Autoimmune Diseases: Contribution of Gut Microbiome.Frontiers in immunology · 2019Review
- IL-17 in Renal Immunity and Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2018Review
- Fisetin inhibits pristine-induced systemic lupus erythematosus in a murine model through CXCLs regulation.International journal of molecular medicine · 2018Article
- Article
- RORγt expression in TClinical and experimental immunology · 2017Article
- Adjuvants- and vaccines-induced autoimmunity: animal models.Immunologic research · 2017Article
- IL-17F Promotes Tissue Injury in Autoimmune Kidney Diseases.Journal of the American Society of Nephrology : JASN · 2016Article
- Suppression of interleukin 17 contributes to the immunomodulatory effects of adipose-derived stem cells in a murine model of systemic lupus erythematosus.Immunologic research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-17A is increased both in serum and in kidney biopsies from patients with lupus nephritis, but direct evidence of pathogenicity is less well established. Administration of pristane to genetically intact mice results in the production of autoantibodies and proliferative glomerulonephritis, resembling human lupus nephritis. These studies sought to define the role of IL-17A in experimental lupus induced by pristane administration. Pristane was administered to wild-type (WT) and IL-17A(-/-) mice. Local and systemic immune responses were assessed after 6 days and 8 weeks, and autoimmunity, glomerular inflammation and renal injury were measured at 7 months. IL-17A production increased significantly 6 days after pristane injection, with innate immune cells, neutrophils (Ly6G(+)) and macrophages (F4/80(+)) being the predominant source of IL-17A. After 8 weeks, while systemic IL-17A was still readily detected in WT mice, the levels of proinflammatory cytokines, interferon (IFN)-γ and tumour necrosis factor (TNF) were diminished in the absence of endogenous IL-17A. Seven months after pristane treatment humoral autoimmunity was diminished in the absence of IL-17A, with decreased levels of immunoglobulin (Ig)G and anti-dsDNA antibodies. Renal inflammation and injury was less in the absence of IL-17A. Compared to WT mice, glomerular IgG, complement deposition, glomerular CD4(+) T cells and intrarenal expression of T helper type 1 (Th1)-associated proinflammatory mediators were decreased in IL-17A(-/-) mice. WT mice developed progressive proteinuria, but functional and histological renal injury was attenuated in the absence of IL-17A. Therefore, IL-17A is required for the full development of autoimmunity and lupus nephritis in experimental SLE, and early in the development of autoimmunity, innate immune cells produce IL-17A.
Indexed as
Identifiers
What OpenQuestion holds
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.