Evidence map›Paper›PMID 10712436›Full record

ArticleThe Journal of clinical investigation2000

CD28-B7 blockade prevents the development of experimental autoimmune glomerulonephritis.

J Reynolds, F W Tam, A Chandraker, J Smith, A M Karkar, J Cross, R Peach, M H Sayegh, C D Pusey

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 175 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. 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
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Inflammatory processes in renal fibrosis.Nature reviews. Nephrology · 2014
    Review
  17. The HLA-DRB1*15:01-restricted Goodpasture's T cell epitope induces GN.Journal of the American Society of Nephrology : JASN · 2013
    Article
  18. Antibodies against linear epitopes on the Goodpasture autoantigen and kidney injury.Clinical journal of the American Society of Nephrology : CJASN · 2012
    Article
  19. Cutting edge issues in Goodpasture's disease.Clinical reviews in allergy & immunology · 2011
    Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

J ReynoldsDivision of Medicine, Imperial College School of Medicine, Hammersmith Hospital, London W12 ONN, United Kingdom. john.reynolds@ic.ac.uk
F W Tam
A Chandraker
J Smith
A M Karkar
J Cross
R Peach
M H Sayegh
C D Pusey
Hammersmith Hospital · GBBrigham and Women's Hospital · USBristol-Myers Squibb (United States) · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Experimental autoimmune glomerulonephritis (EAG), an animal model of Goodpasture's disease, can be induced in Wistar Kyoto (WKY) rats by a single injection of rat glomerular basement membrane (GBM) in adjuvant. EAG is characterized by circulating and deposited anti-GBM antibodies, accompanied by focal necrotizing glomerulonephritis with crescent formation. The role of T cells in the pathogenesis of EAG remains unclear. T-cell costimulation is provided by ligation of CD28 with either B7.1 (CD80) or B7.2 (CD86) on antigen-presenting cells, and can be inhibited by a soluble form of CTLA4 (CTLA4-Ig) that binds to both B7.1 and B7.2. We examined the effect of CD28-B7 blockade on the development of EAG using native CTLA4-Ig or mutant CTLA4-Ig (Y100F-Ig), which selectively blocks B7.1. Native CTLA4-Ig treatment ameliorated EAG by several measures, including the levels of circulating anti-GBM antibodies, albuminuria, the deposition of IgG and fibrin in the glomeruli, the severity of glomerular abnormalities, and the numbers of infiltrating T cells and macrophages. Y100F-Ig resulted in a similar reduction in the severity of nephritis, but produced no overall reduction in circulating anti-GBM antibodies, although there was a reduction in IgG2a antibodies. We concluded that CD28-B7 blockade reduced autoantibody production and cellular infiltration of glomeruli, and prevented target organ injury. Our results suggest a key role for B7. 1 in costimulation of Th1-like autoimmune responses in the rat, and show that glomerular injury in EAG is largely dependent on cell-mediated mechanisms.

Indexed as

ImmunoconjugatesAbataceptAnimalsAntigens, CDAntigens, DifferentiationAnti-Glomerular Basement Membrane DiseaseAutoantibodiesAutoimmune DiseasesB7-1 AntigenBasement MembraneCD28 AntigensCTLA-4 AntigenDisease Models, AnimalFibrinFluorescent Antibody TechniqueGlomerulonephritisAbataceptAntigens, CDAntigens, DifferentiationAutoantibodiesB7-1 AntigenCD28 AntigensCTLA-4 AntigenCtla4 protein, ratFibrinImmunoconjugatesImmunoglobulin G

Identifiers

PMID10712436
PMCPMC289170
OpenAlexW2075048150

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.