Evidence map›Paper›PMID 15254597›Full record

ArticleThe Journal of clinical investigation2004

Th2-predominant inflammation and blockade of IFN-gamma signaling induce aneurysms in allografted aortas.

Koichi Shimizu, Masayoshi Shichiri, Peter Libby, Richard T Lee, Richard N Mitchell

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
8.9field-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

104 citing papers in PubMed, 199 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Causal associations between 17 common autoimmune diseases and aortic diseases: a Mendelian randomization study.International journal of cardiology. Cardiovascular risk and prevention · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Role of Extracellular Matrix and Inflammation in Abdominal Aortic Aneurysm.International journal of molecular sciences · 2022
    Review
  17. Review
  18. Pathogenic Tconvs promote inflammatory macrophage polarization through GM-CSF and exacerbate abdominal aortic aneurysm formation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  19. Review
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 3 countries.

Koichi ShimizuThe Donald W. Reynolds Cardiovascular Clinical Research Center, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. ksmz@rics.bwh.harvard.edu
Masayoshi Shichiri
Peter Libby
Richard T Lee
Richard N Mitchell
Brigham and Women's Hospital · USCardiovascular Research Center · BRTokyo Medical and Dental University · JP

Funding

The IL-18/Caspase-1 cascade in atherosclerosisR01HL067283 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI SHI, GUO-PING · 2003 to 2006
$1.6M
Inflammation and Aortic Aneurysm PathophysiologyR01HL067249 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI SUKHOVA, GALINA K · 2003 to 2006
$1.5M
Origin of Intimal cells in allograft arteriopathyR01GM067049 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI MITCHELL, RICHARD N · 2003 to 2006
$1.4M
PATHOGENESIS OF TRANSPLANT-ASSOCIATED ARTERIOSCLEROSISR01HL043364 · NHLBI · TUFTS MEDICAL CENTER · PI MITCHELL, RICHARD N · 1990 to 2003
$1.2M
NHLBI NIH HHS HL-67249NHLBI NIH HHS R01 HL067283NHLBI NIH HHS R01 HL-43364NIGMS NIH HHS GM-67049NIGMS NIH HHS R01 GM067049
6 · The paper itself

Abstract

Abdominal aortic aneurysms (AAAs) cause death due to complications related to expansion and rupture. The underlying mechanisms that drive AAA development remain largely unknown. We recently described evidence for a shift toward T helper type 2 (Th2) cell responses in human AAAs compared with stenotic atheromas. To evaluate putative pathways in AAA formation, we induced Th1- or Th2-predominant cytokine environments in an inflammatory aortic lesion using murine aortic transplantation into WT hosts or those lacking the receptors for the hallmark Th1 cytokine IFN-gamma, respectively. Allografts in WT recipients developed intimal hyperplasia, whereas allografts in IFN-gamma receptor-deficient (GRKO) hosts developed severe AAA formation associated with markedly increased levels of MMP-9 and MMP-12. Allografts in GRKO recipients treated with anti-IL-4 antibody to block the characteristic IL-4 Th2 cytokine or allografts in GRKO hosts also congenitally deficient in IL-4 did not develop AAA and likewise exhibited attenuated collagenolytic and elastolytic activities. These observations demonstrate an important dichotomy between cellular immune responses that induce IFN-gamma- or IL-4-dominated cytokine environments. The findings establish important regulatory roles for a Th1/Th2 cytokine balance in modulating matrix remodeling and have important implications for the pathophysiology of AAAs and arteriosclerosis.

Indexed as

AnimalsAorta, AbdominalAortic Aneurysm, AbdominalCD11b AntigenCD4-Positive T-LymphocytesHumansInflammationInterferon-gammaInterferon gamma ReceptorInterleukin-4MacrophagesMatrix MetalloproteinasesMiceMice, Inbred StrainsMice, KnockoutReceptors, InterferonCD11b AntigenInterferon-gammaInterferon gamma ReceptorInterleukin-4Matrix MetalloproteinasesReceptors, InterferonRNA, Messenger

Identifiers

PMID15254597
PMCPMC449742
OpenAlexW2157764570

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.