ArticleThe Journal of clinical investigation2005
Renal cell-expressed TNF receptor 2, not receptor 1, is essential for the development of glomerulonephritis.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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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.
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Who cites it
60 citing papers in PubMed, 116 citations in OpenAlex.
- Systematic prioritization of potential therapeutic targets for glomerulonephritis using multi-omics Mendelian randomization.PLoS computational biology · 2026Article
- Integrative RNA-seq and CLIP-seq analysis revealsFrontiers in physiology · 2025Article
- Pathogenesis of HIV-associated nephropathy in children and adolescents: taking a hard look 40 years later in the era of gene-environment interactions.American journal of physiology. Renal physiology · 2024Review
- Role of baseline soluble tumor necrosis factor receptor 2 as a biomarker in primary podocytopathy: Implications for renal impairment and disease progression.BMC nephrology · 2024Article
- Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- TNFR2 as a Potential Biomarker for Early Detection and Progression of CKD.Biomolecules · 2023Article
- Gut region-specific TNFR expression: TNFR2 is more affected than TNFR1 in duodenal myenteric ganglia of diabetic rats.World journal of diabetes · 2023Article
- Responses to Ang II (Angiotensin II), Salt Intake, and Lipopolysaccharide Reveal the Diverse Actions of TNF-α (Tumor Necrosis Factor-α) on Blood Pressure and Renal Function.Hypertension (Dallas, Tex. : 1979) · 2022Review
- The therapeutic effects of human embryonic stem cells-derived immunity-and-matrix regulatory cells on membranous nephropathy.Stem cell research & therapy · 2022Article
- Inflammatory biomarkers in staging of chronic kidney disease: elevated TNFR2 levels accompanies renal function decline.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Monocytes transition to macrophages within the inflamed vasculature via monocyte CCR2 and endothelial TNFR2.The Journal of experimental medicine · 2022Article
- The Signaling Pathway of TNF Receptors: Linking Animal Models of Renal Disease to Human CKD.International journal of molecular sciences · 2022Review
- Context-dependent induction of autoimmunity by TNF signaling deficiency.JCI insight · 2022Article
- Targeting Differential Roles of Tumor Necrosis Factor Receptors as a Therapeutic Strategy for Glaucoma.Frontiers in immunology · 2022Review
- Influence of anti-TNF-α treatment on liver and kidney functions in patients with ankylosing spondylitis: A retrospective longitudinal study.European journal of rheumatology · 2022Article
- AMPK mediates regulation of glomerular volume and podocyte survival.JCI insight · 2021Article
- Plasma Biomarkers of Tubular Injury and Inflammation Are Associated with CKD Progression in Children.Journal of the American Society of Nephrology : JASN · 2020Article
- Increased circulating cytokine levels in African American women with obesity and elevated HbA1c.Cytokine · 2020Article
- Circulating Tumor Necrosis Factor Receptors: A Potential Biomarker for the Progression of Diabetic Kidney Disease.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
TNF is essential for the development of glomerulonephritis, an immune-mediated disorder that is a major cause of renal failure worldwide. However, TNF has proinflammatory and immunosuppressive properties that may segregate at the level of the 2 TNF receptors (TNFRs), TNFR1 and TNFR2. TNFR1-deficient mice subjected to immune complex-mediated glomerulonephritis developed less proteinuria and glomerular injury, and fewer renal leukocyte infiltrates at early time points after disease induction, and this was associated with a reduced systemic immune response to nephrotoxic rabbit IgG. However, proteinuria and renal pathology were similar to those in wild-type controls at later time points, when lack of TNFR1 resulted in excessive renal T cell accumulation and an associated reduction in apoptosis of these cells. In sharp contrast, TNFR2-deficient mice were completely protected from glomerulonephritis at all time points, despite an intact systemic immune response. TNFR2 was induced on glomerular endothelial cells of nephritic kidneys, and TNFR2 expression on intrinsic cells, but not leukocytes, was essential for glomerulonephritis and glomerular complement deposition. Thus, TNFR1 promotes systemic immune responses and renal T cell death, while intrinsic cell TNFR2 plays a critical role in complement-dependent tissue injury. Therefore, therapeutic blockade specifically of TNFR2 may be a promising strategy in the treatment of immune-mediated glomerulonephritis.
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