ReviewNature reviews. Nephrology2017
T cells and autoimmune kidney disease.
Review in Nature reviews. Nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.
What it found
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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.
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
75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 134 citations in OpenAlex.
- Efficacy of Tripterygium glycosides in immune-mediated kidney diseases as a immunomodulation drug in combination with conventional immunosuppressive agents: a systematic review and meta-analysis of randomized controlled trials.Frontiers in pharmacology · 2025Pooled it
- Renal manifestations in inflammatory bowel disease: a systematic review.Journal of gastroenterology · 2022Pooled it
- Efficacy and safety of low-dose IL-2 in the treatment of systemic lupus erythematosus: a randomised, double-blind, placebo-controlled trial.Annals of the rheumatic diseases · 2020Trial
- CD4 + T cell-derived exosomal miR-223-3p serves as a potential biomarker for systemic lupus erythematosus and attenuates lupus nephritis in NZBWF1/J mice.Journal of nanobiotechnology · 2026Article
- [Research progress on the application of telitacicept in rheumatism and autoimmune diseases].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Review
- Can we cure autoimmunity?Current opinion in immunology · 2026Review
- The Interplay Between Rheumatoid Arthritis and Chronic Kidney Disease: From Mechanisms to Treatment.Journal of clinical medicine · 2025Review
- Cre-driven tdTomato expression unexpectedly confers resistance to peripheral but not central lupus in dLckCre mice.Journal of translational autoimmunity · 2025Article
- CAR-T Cell Therapy for Autoimmune Kidney Diseases: Where Do We Stand Now?International journal of molecular sciences · 2025Review
- Taming renal inflammation: signaling pathways and therapeutic advances in lupus nephritis.BMC nephrology · 2025Review
- Butyrophilin 3A1 Contributes to Inflammation and Induces a Lupus-Like Disease by Inhibiting the IL-38-Ferroptosis Axis.MedComm · 2025Article
- Circulating T cell atlas in Moyamoya disease: insights into immunopathogenesis of cerebrovascular disorders.Journal of neuroinflammation · 2025Article
- Kidney immunology from pathophysiology to clinical translation.Nature reviews. Immunology · 2025Review
- IL-12 family cytokines and autoimmune diseases: A potential therapeutic target?Journal of translational autoimmunity · 2025Review
- Type I interferon drives T cell cytotoxicity by upregulation of interferon regulatory factor 7 in autoimmune kidney diseases in mice.Nature communications · 2025Article
- Immune inflammation and metabolic interactions in the pathogenesis of diabetic nephropathy.Frontiers in endocrinology · 2025Review
- Revolutionizing Autoimmune Kidney Disease Treatment with Chimeric Antigen Receptor-T Cell Therapy.Research (Washington, D.C.) · 2025Review
- Podocyte, tubular epithelial-immune cell interplay in the pathogenesis of lupus nephritis.Frontiers in immunology · 2025Review
- Insights into renal and urological complications of inflammatory bowel disease.World journal of nephrology · 2024Review
- Membranous nephropathy: pathogenesis and treatments.MedComm · 2024Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glomerulonephritis is traditionally considered to result from the invasion of the kidney by autoantibodies and immune complexes from the circulation or following their formation in situ, and by cells of the innate and the adaptive immune system. The inflammatory response leads to the proliferation and dysfunction of cells of the glomerulus, and invasion of the interstitial space with immune cells, resulting in tubular cell malfunction and fibrosis. T cells are critical drivers of autoimmunity and related organ damage, by supporting B-cell differentiation and antibody production or by directly promoting inflammation and cytotoxicity against kidney resident cells. T cells might become activated by autoantigens in the periphery and become polarized to secrete inflammatory cytokines before entering the kidney where they have the opportunity to expand owing to the presence of costimulatory molecules and activating cytokines. Alternatively, naive T cells could enter the kidney where they become activated after encountering autoantigen and expand locally. As not all individuals with a peripheral autoimmune response to kidney antigens develop glomerulonephritis, the contribution of local kidney factors expressed or produced by kidney cells is probably of crucial importance. Improved understanding of the biochemistry and molecular biology of T cells in patients with glomerulonephritis offers unique opportunities for the recognition of treatment targets for autoimmune kidney disease.
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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.