Evidence map›Paper›PMID 15972947›Full record

ArticleThe American journal of pathology2005

Protection against experimental autoimmune myocarditis is mediated by interleukin-10-producing T cells that are controlled by dendritic cells.

Ya Li, Janet S Heuser, Stanley D Kosanke, Mark Hemric, Madeleine W Cunningham

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Regulatory Role of CD4Journal of immunology research · 2018
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. TLR3 deficiency induces chronic inflammatory cardiomyopathy in resistant mice following coxsackievirus B3 infection: role for IL-4.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
    Article
  12. Article
  13. Article
  14. Autoimmune myocarditis, valvulitis, and cardiomyopathy.Current protocols in immunology · 2013
    Article
  15. Article
  16. Article
  17. 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

5 authors at 1 institution in 1 country.

Ya LiDepartment of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
Janet S Heuser
Stanley D Kosanke
Mark Hemric
Madeleine W Cunningham
University of Oklahoma Health Sciences Center · US

Funding

AUTOIMMUNE DETERMINANTS OF HUMAN CARDIAC MYOSINR01HL056267 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI COOPER, LESLIE T, CUNNINGHAM, MADELEINE W. · 1997 to 2013
$4.7M
Autoimmune Determinants of Human Cardiac MyosinR56HL056267 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI COOPER, LESLIE T, CUNNINGHAM, MADELEINE W. · 2008 to 2015
$933k
NHLBI NIH HHS HL 56267NHLBI NIH HHS R01 HL056267NHLBI NIH HHS R56 HL056267
6 · The paper itself

Abstract

Experimental autoimmune myocarditis (EAM) can be induced in the Lewis rat by cardiac myosin or its cryptic S2-16 peptide epitope (amino acids 1052 to 1076). To investigate cellular mechanisms and the role of antigen-presenting cells in regulation of myocarditis, we induced protection against EAM in Lewis rats by administration of S2-16 peptide in incomplete Freund's adjuvant (IFA). Protection to EAM was associated with activation of S2-16-reactive splenocytes secreting high levels of interleukin (IL)-10 and reduced levels of interferon-gamma and IL-2. Adoptive transfer of S2-16:IFA-induced splenocytes producing IL-10 suppressed myocarditis induction in syngeneic recipients, suggesting their regulatory cell nature. However, exposure of S2-16:IFA-induced cells to inflammatory cytokine IL-12 converted them to Th1 effectors that transferred EAM. Differentiated function of S2-16-reactive T cells in protected rats resulted from increased IL-10 production by dendritic cells (DCs). Purified DCs from S2-16:IFA-treated rats promoted S2-16-reactive CD4+ T cells to produce increased IL-10 and reduced interferon-gamma. In addition, adoptive transfer of IL-10-producing DCs from S2-16:IFA-treated rats also induced protection to EAM in recipient rats. These studies demonstrated DCs and key cytokines, such as IL-10 and IL-12, regulated the fate of T cells in myocarditis development in the Lewis rat.

Indexed as

Adoptive TransferAnimalsAntigen-Presenting CellsAutoimmune DiseasesCardiac MyosinsCell ProliferationDendritic CellsFemaleFlow CytometryImmunomagnetic SeparationInterferon-gammaInterleukin-10Interleukin-12MyocarditisRatsRats, Inbred LewCardiac MyosinsInterferon-gammaInterleukin-10Interleukin-12

Identifiers

PMID15972947
PMCPMC1603447
OpenAlexW1964025326

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.