Evidence map›Paper›PMID 19811893›Full record

ArticleJournal of autoimmunity

Spontaneous autoimmune myocarditis and cardiomyopathy in HLA-DQ8.NODAbo transgenic mice.

Veena Taneja, Chella S David

Abstract read
In one paragraph

Article in Journal of autoimmunity. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Immune checkpoint inhibitor-associated myocarditis: clinical and mechanistic insights.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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  4. Article
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  12. Do Genes Influence Susceptibility to Myocarditis?JACC. Basic to translational science · 2021
    Article
  13. Review
  14. Article
  15. Review
  16. Regulatory Role of CD4Journal of immunology research · 2018
    Review
  17. Review
  18. Article
  19. FTY720 (Gilenya) treatment prevents spontaneous autoimmune myocarditis and dilated cardiomyopathy in transgenic HLA-DQ8-BALB/c mice.Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
    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

2 authors at 2 institutions in 1 country.

Veena TanejaDepartment of Immunology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. taneja.veena@mayo.edu
Chella S David
Mayo Clinic · USMayo Clinic in Arizona · US

Funding

IMMUNOGENETICS OF COLLAGEN-INDUCED ARTHRITIS IN MICER01AR030752 · NIAMS · MAYO CLINIC ROCHESTER · PI DAVID, CHELLA S, TANEJA, VEENA · 1987 to 2014
$4.3M
Role of B cells in pathogenesis of Collagen-induced Arthritis in Humanized MiceR01AI075262 · NIAID · MAYO CLINIC ROCHESTER · PI TANEJA, VEENA · 2009 to 2012
$1.2M
NIAID NIH HHS R01 AI075262NIAMS NIH HHS R01 AR030752
6 · The paper itself

Abstract

Most individuals have viral infections at some point in their life, however, only few develop autoreactivity to cardiac myosin following infection suggesting a genetic predisposition. Population studies have shown that among all the genetic factors linked with autoimmune disease development, MHC class II genes are the most significant genetic factors. Experimental autoimmune myocarditis resembling human Dilated cardiomyopathy can be induced in susceptible mice by infection with coxsackie virus as well as immunization with purified foreign and murine cardiac specific a-myosin. We generated transgenic mice lacking endogenous class II molecules, HLA-DR3.Abo and HLA-DQ8.Abo transgenic mice in NOD and HLA-DQ8.Abo in B10 background, to study the role of MHC in spontaneous autoimmunity. The HLA molecules in these mice are expressed on cell surface and can positively select CD4+ T cells expressing various Vb T cell receptors. NOD.DQ8 female mice spontaneously developed myocarditis and dilated cardiomyopathy. Histopathology of heart revealed mononuclear infiltrate consisting of CD4 and Mac-1+ cells and myocyte necrosis. NOD.DQ8 mice showed cellular and humoral autoreactive response to self cardiac myosin.. Depletion of CD8 and CD4 + cells suggested that CD8 T cells may act as regulatory cells while CD4 cells are required as effector cells. NOD.DR3 and B10.DQ8 mice did not develop any cardiac pathology suggesting DQ8 is required for predisposition to the spontaneous autoreactivity while NOD background influences onset and progression of disease. Thus these mice provide powerful tools to understand the role of HLA class II molecules in predisposition and onset of human diseases and to develop immunotherapy.

Indexed as

Disease Models, AnimalMiceAnimalsAutoantibodiesAutoimmune DiseasesCardiac MyosinsCardiomyopathy, DilatedCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCytokinesFemaleHLA-DQ AntigensHumansMaleMice, Inbred NODMice, KnockoutAutoantibodiesCardiac MyosinsCytokinesHLA-DQ8 antigenHLA-DQ Antigens

Identifiers

PMID19811893
PMCPMC3574900
OpenAlexW2036751727

What OpenQuestion holds

Textmetadata
LicenceTDM
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.