ArticleThe Journal of clinical investigation2009
Focal and segmental glomerulosclerosis induced in mice lacking decay-accelerating factor in T cells.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
- Trial
- Deletion of decay-accelerating factor in kidney tubular cells mitigates kidney fibrosis in aristolochic acid nephropathy.American journal of physiology. Renal physiology · 2026Article
- Cytokine-Driven Janus Kinase Signal Transducer and Activator of Transcription Pathway Hyperactivity Predicts Disease Severity in Pediatric FSGS.Kidney360 · 2026Article
- Reduced decay-accelerating factor expression promotes complement-mediated cystogenesis in murine ADPKD.JCI insight · 2024Article
- Article
- CD8 T Cell-Derived Exosomal miR-186-5p Elicits Renal Inflammation via Activating Tubular TLR7/8 Signal Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Current understanding of the molecular mechanisms of circulating permeability factor in focal segmental glomerulosclerosis.Frontiers in immunology · 2023Review
- Loss of decay-accelerating factor triggers podocyte injury and glomerulosclerosis.The Journal of experimental medicine · 2020Article
- Role of Podocyte Injury in Glomerulosclerosis.Advances in experimental medicine and biology · 2019Review
- JAK-STAT signaling is activated in the kidney and peripheral blood cells of patients with focal segmental glomerulosclerosis.Kidney international · 2018Article
- Complement in Non-Antibody-Mediated Kidney Diseases.Frontiers in medicine · 2017Review
- Molecules Great and Small: The Complement System.Clinical journal of the American Society of Nephrology : CJASN · 2015Review
- The experimental model of nephrotic syndrome induced by Doxorubicin in rodents: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015Review
- A 7-year-old boy with renal insufficiency and proteinuria after stem cell transplant for T-cell acute lymphoblastic leukemia.Clinical nephrology · 2014Article
- Progenitor cells and podocyte regeneration.Seminars in nephrology · 2014Review
- Decay-accelerating factor 1 deficiency exacerbates leptospiral-induced murine chronic nephritis and renal fibrosis.PloS one · 2014Article
- The role of the immune system in idiopathic nephrotic syndrome: a review of clinical and experimental studies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Review
- Complement regulation in renal disease models.Seminars in nephrology · 2013Review
- Complement regulation of T-cell alloimmunity.Seminars in nephrology · 2013Review
- Podocytes are nonhematopoietic professional antigen-presenting cells.Journal of the American Society of Nephrology : JASN · 2013Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Heritable and acquired diseases of podocytes can result in focal and segmental glomerulosclerosis (FSGS). We modeled FSGS by passively transferring mouse podocyte-specific sheep Abs into BALB/c mice. BALB/c mice deficient in the key complement regulator, decay-accelerating factor (DAF), but not WT or CD59-deficient BALB/c mice developed histological and ultrastructural features of FSGS, marked albuminuria, periglomerular monocytic and T cell inflammation, and enhanced T cell reactivity to sheep IgG. All of these findings, which are characteristic of FSGS, were substantially reduced by depleting CD4+ T cells from Daf(-/-) mice. Furthermore, WT kidneys transplanted into Daf(-/-) recipients and kidneys of DAF-sufficient but T cell-deficient Balb/(cnu/nu) mice reconstituted with Daf(-/-) T cells developed FSGS. In contrast, DAF-deficient kidneys in WT hosts and Balb/(cnu/nu) mice reconstituted with DAF-sufficient T cells did not develop FSGS. Thus, we have described what we believe to be a novel mouse model of FSGS attributable to DAF-deficient T cell immune responses. These findings add to growing evidence that complement-derived signals shape T cell responses, since T cells that recognize sheep Abs bound to podocytes can lead to cellular injury and development of FSGS.
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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.