Evidence map›Paper›PMID 18275831›Full record

ArticleImmunity2008

Combined deficiency of proapoptotic regulators Bim and Fas results in the early onset of systemic autoimmunity.

Jack Hutcheson, John C Scatizzi, Akbar M Siddiqui, G Kenneth Haines, Tianfu Wu, Quan-Zhen Li, Laurie S Davis, Chandra Mohan, Harris Perlman

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 2 pooled it
9.3field-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

133 citing papers in PubMed, 2 syntheses or guidelines pooled it, 219 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Mechanisms and Therapeutic Implications of EZH2 in Nasal Diseases.Clinical reviews in allergy & immunology · 2025
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. CD95/Fas ligand induced toxicity.Biochemical Society transactions · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

73 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 2 countries.

Jack HutchesonDepartment of Molecular Microbiology & Immunology, School of Medicine, Saint Louis University, Saint Louis, MO 63104, USA.
John C Scatizzi
Akbar M Siddiqui
G Kenneth Haines
Tianfu Wu
Quan-Zhen Li
Laurie S Davis
Chandra Mohan
Harris Perlman
Southwestern Medical CenterSaint Louis University · USUCLouvain Saint-Louis Brussels · BEUniversity of California San Diego · USYale University · US

Funding

Virology and Smallpox VaccinationsU54AI057160 · NIAID · WASHINGTON UNIVERSITY · PI RAY, RANJIT · 2003 to 2013
$80.9M
Therapeutic Role for P21 in Suppressing IL-1 Beta Mediated PathologiesR01AR050250 · NIAMS · SAINT LOUIS UNIVERSITY · PI PERLMAN, HARRIS R · 2003 to 2014
$3.0M
TH-1 BIAS IN RHEUMATOID ARTHRITISR01AR045293 · NIAMS · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI DAVIS, LAURIE S · 1999 to 2003
$1.1M
The role BH3 and multi BH domain genes in regulating monocyte survival and functiR21AI067590 · NIAID · SAINT LOUIS UNIVERSITY · PI PERLMAN, HARRIS R · 2007 to 2008
$407k
NIAID NIH HHS AI 067590NIAID NIH HHS U54 AI 057160NIAMS NIH HHS AR 050250NIAMS NIH HHS AR 45293
6 · The paper itself

Abstract

Alterations in the stoichiometric balance between members of Bcl-2 and Fas apoptotic pathway could lead to the pathogenesis of systemic lupus erythematosus (SLE). We showed that patients with SLE displayed increased expression in antiapoptotic members of the Bcl-2 and Fas apoptotic pathways in isolated mononuclear cells. Further, mice (Bcl2l11(-/-)Fas(lpr/lpr)) lacking the Bcl-2 pro-apoptotic member, Bim (Bcl2l11(-/-)) and and with an lpr mutation in the gene encoding Fas (Fas(lpr/lpr)) developed severe SLE-like disease by 16 weeks of age unlike Bcl2l11(-/-) or Fas(lpr/lpr) mice. Bcl2l11(-/-)Fas(lpr/lpr) antigen-presenting cells (APCs) were markedly activated, and their numbers were increased in lymphoid tissues and in kidneys, yet numerous TUNEL-positive cells were observed in glomeruli of Bcl2l11(-/-)Fas(lpr/lpr) mice. These data demonstrate that dysregulation of the Bcl-2 or Fas pathways can alter the function of APCs, thereby leading to SLE pathogenesis.

Indexed as

ApoptosisAutoimmunityAnimalsAntigen-Presenting CellsApoptosis Regulatory ProteinsAutoantibodiesBcl-2-Like Protein 11B-Lymphocytesfas ReceptorHumansKidneyLupus Erythematosus, SystemicLymphatic DiseasesMacrophage ActivationMacrophagesMembrane ProteinsApoptosis Regulatory ProteinsAutoantibodiesBCL2L11 protein, humanBcl2l11 protein, mouseBcl-2-Like Protein 11fas ReceptorMembrane ProteinsProto-Oncogene Proteins

Identifiers

PMID18275831
OpenAlexW2093718923

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.