Evidence map›Paper›PMID 9815255›Full record

ArticleThe Journal of experimental medicine1998

Permanent CD8(+) T cell depletion prevents proteinuria in active Heymann nephritis.

M J Penny, R A Boyd, B M Hall

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. 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
  6. Alloactivation of Naïve CD4Frontiers in immunology · 2019
    Article
  7. Article
  8. Article
  9. Article
  10. T Cells: Soldiers and Spies--The Surveillance and Control of Effector T Cells by Regulatory T Cells.Clinical journal of the American Society of Nephrology : CJASN · 2015
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Production of a new model of slowly progressive Heymann nephritis.International journal of experimental pathology · 2003
    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

3 authors at 2 institutions in 1 country.

M J PennyDepartment of Medicine, Liverpool Hospital and the University of New South Wales, Liverpool, New South Wales 2170, Australia. pennymark@bigpond.com
R A Boyd
B M Hall
UNSW Sydney · AULiverpool Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Active Heymann nephritis (HN) is a rat model of human idiopathic membranous nephropathy in which injury is thought to be mediated by membrane attack complex of complement (MAC) activated by antibody (Ab) to glomerular epithelial cells. Recent work has shown that HN develops in C6-deficient rats which cannot assemble MAC, and that infiltration of activated cytotoxic CD8(+) T cells and macrophages into glomeruli coincides with proteinuria. This study examined the role of CD8(+) T cells in mediating glomerular injury in HN by permanent CD8(+) cytotoxic T cell depletion via adult thymectomy (ATx) and anti-CD8 mAb. Groups of rats were depleted of CD8(+) T cells either before immunization for HN or 6 wk after immunization when Ab responses and glomerular IgG deposition were well established. These were compared with groups of HN, ATx/HN, and complete Freund's adjuvant (CFA) controls. Neither group of CD8(+) T cell-depleted rats developed proteinuria, although there was normal development and deposition of Ab. CD8(+) T cell-depleted rats developed neither T cell or macrophage infiltrates nor their effector cytokines, which are present in glomeruli of rats with HN. Examination of lymph node (LN) draining sites of immunization showed these findings were not explained by altered immune events within these LNs. It was concluded that CD8(+) cytotoxic T cells are essential to the mediation of glomerular injury in HN and may be relevant to the pathogenesis and treatment of membranous nephropathy.

Indexed as

AnimalsAntibodies, MonoclonalCD3 ComplexCD8-Positive T-LymphocytesCytokinesDisease Models, AnimalGlomerulonephritisHistocytochemistryImmunoglobulin GKidney GlomerulusLymph NodesMaleProteinuriaRatsRats, Inbred LewRNA, MessengerAntibodies, MonoclonalCD3 ComplexCytokinesImmunoglobulin GRNA, Messenger

Identifiers

PMID9815255
PMCPMC2212409
OpenAlexW2164808616

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.