Evidence map›Paper›PMID 19470687›Full record

ArticleJournal of the American Society of Nephrology : JASN2009

Invariant natural killer T cells and TGF-beta attenuate anti-GBM glomerulonephritis.

Laurent Mesnard, Alexandre C Keller, Marie-Laure Michel, Sophie Vandermeersch, Cédric Rafat, Emmanuel Letavernier, Yves Tillet, Eric Rondeau, Maria C Leite-de-Moraes

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Metabolic signatures of immune cells in chronic kidney disease.Expert reviews in molecular medicine · 2022
    Review
  6. Article
  7. Unconventional T cells and kidney disease.Nature reviews. Nephrology · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Roles of Natural Killer T Cells and Natural Killer Cells in Kidney Injury.International journal of molecular sciences · 2019
    Review
  12. Article
  13. Tissue-Resident Lymphocytes in the Kidney.Journal of the American Society of Nephrology : JASN · 2018
    Review
  14. Article
  15. Review
  16. NFJournal of the American Society of Nephrology : JASN · 2017
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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 6 institutions in 4 countries.

Laurent MesnardINSERM, UMR S 702, Hôpital Tenon, Paris, France.
Alexandre C Keller
Marie-Laure Michel
Sophie Vandermeersch
Cédric Rafat
Emmanuel Letavernier
Yves Tillet
Eric Rondeau
Maria C Leite-de-Moraes
Hôpital Tenon · FRUniversité du Burundi · BICentre National de la Recherche Scientifique · FRInserm · FRPhysiologie de la Reproduction et des Comportements · FRSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Invariant natural killer T (iNKT) cells represent a particular subset of T lymphocytes capable of producing several cytokines, which exert regulatory or effector functions, following stimulation of the T cell receptor. In this study, we investigated the influence of iNKT cells on the development of experimental anti-glomerular basement membrane glomerulonephritis (anti-GBM GN). After injection of anti-GBM serum, the number of kidney iNKT cells rapidly increased. iNKT cell-deficient mice (Jalpha18-/-) injected with anti-GBM serum demonstrated worse renal function, increased proteinuria, and greater glomerular and tubular injury compared with similarly treated wild-type mice. We did not detect significant differences in Th1/Th2 polarization in renal tissue that might have explained the severity of disease in Jalpha18-/- mice. Interestingly, expression of both TGF-beta and TGF-beta-induced (TGFBI) mRNA was higher in wild-type kidneys compared with Jalpha18-/- kidneys, suggesting a possible protective role for TGF-beta in anti-GBM GN. Administration of an anti-TGF-beta neutralizing antibody significantly enhanced the severity of disease in wild-type, but not Jalpha18-/-, mice. In conclusion, in experimental anti-GBM GN, iNKT cells attenuate disease severity and TGF-beta has a renoprotective role.

Indexed as

AnimalsAntibodies, MonoclonalAnti-Glomerular Basement Membrane DiseasebetaIG-H3 ProteinExtracellular Matrix ProteinsKidneyMiceMice, Inbred C57BLMice, KnockoutNatural Killer T-CellsT-Lymphocytes, Helper-InducerTransforming Growth Factor betaAntibodies, MonoclonalbetaIG-H3 ProteinExtracellular Matrix ProteinsTransforming Growth Factor beta

Identifiers

PMID19470687
PMCPMC2689902
OpenAlexW2101375867

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.