Evidence map›Paper›PMID 11854324›Full record

ArticleThe Journal of clinical investigation2002

CD4(+) T cells specific to a glomerular basement membrane antigen mediate glomerulonephritis.

Jean Wu, John Hicks, Jason Borillo, William F Glass, Ya-Huan Lou

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.3field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

51 citing papers in PubMed, 141 citations in OpenAlex.

  1. Article
  2. Article
  3. ET-3/ETBR Mediates NaCirculation research · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Atypical Anti-Glomerular Basement Membrane Disease.Kidney international reports · 2023
    Review
  9. Article
  10. Review
  11. Article
  12. Experimental Antiglomerular Basement Membrane GN Induced by a Peptide fromJournal of the American Society of Nephrology : JASN · 2020
    Article
  13. Role of CD8+ T cells in crescentic glomerulonephritis.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2020
    Review
  14. Article
  15. Article
  16. Goodpasture's autoimmune disease - A collagen IV disorder.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Review
  17. Review
  18. Article
  19. Article
  20. Basement membranes and autoimmune diseases.Matrix biology : journal of the International Society for Matrix Biology · 2017
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Jean WuDepartment of Basic Science, Dental Branch, University of Texas Houston Health Science Center, Houston, Texas 77030, USA.
John Hicks
Jason Borillo
William F Glass
Ya-Huan Lou
Baylor College of Medicine · USEastern Virginia Medical School · USThe University of Texas Health Science Center at Houston · US

Funding

ANTIBODY DIRECTS T CELL MEDIATED AUTOIMMUNITYR01HD035993 · NICHD · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI LOU, YAHUAN · 1999 to 2003
$563k
NICHD NIH HHS R01 HD035993NICHD NIH HHS R01 HD-35993
6 · The paper itself

Abstract

Ab-mediated mechanisms have been considered the major causes of glomerulonephritis (GN). However, recent studies suggest that T cells may be more important in mediating GN. To investigate the effects of antigen-specific CD4(+) T cells, we generated Th1 cell lines specific for this antigen from rats that had been immunized with a recombinant form of the glomerular basement membrane (GBM) antigen, Col4alpha3NC1. Upon the transfer of in vitro-activated T cell lines to pertussis toxin-primed, naive syngeneic rats, the recipients developed severe proteinuria/albuminuria, which plateaued after approximately 35 days. Although no IgG binding to GBM or C3 deposition could be detected by immunofluorescence, five out of eleven rats exhibited severe GN, as judged by the formation of characteristic crescent-shaped lesions in the glomeruli, whereas the others exhibited modest GN. Thus Col4alpha3NC1-specific T cells directly initiated glomerular injury in the recipients. One notable difference from GN induced by active immunization was a T cell infiltration in the renal interstitium, which affected some tubules. We therefore injected fluorescence-labeled Col4alpha3NC1-specific into naive rats, and we found that they were enriched 4.5-fold in the kidney cortex relative to nonspecific control T cells 24 hours later. Many of the T cells were located in the Bowman's space and had a flattened shape, suggesting that the primary target for the T cells was in or adjacent to the Bowman's capsule.

Indexed as

AnimalsAutoantigensBasement MembraneCD4-Positive T-LymphocytesCell LineCollagen Type IVCytokinesFemaleGlomerulonephritisImmunizationKidney GlomerulusLymphocyte ActivationRatsRats, Inbred WKYAutoantigensCollagen Type IVCytokines

Identifiers

PMID11854324
PMCPMC150874
OpenAlexW2004768358

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.