Evidence map›Paper›PMID 23810579›Full record

ReviewJournal of autoimmunity2013

The heart of the matter: protection of the myocardium from T cells.

Andrew H Lichtman

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of autoimmunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 3 pooled it
2.0field-weighted citation impact, top 12% 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

48 citing papers in PubMed, 3 syntheses or guidelines pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
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  8. Review
  9. Immune checkpoint inhibitor-associated myocarditis: a historical and comprehensive review.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Background and roles: myosin in autoimmune diseases.Frontiers in cell and developmental biology · 2023
    Review
  16. Review
  17. Review
  18. Review
  19. Article
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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

1 author at 1 institution in 1 country.

Andrew H LichtmanDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, NRB Room 752N, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. Electronic address: alichtman@partners.org.
Harvard University · US

Funding

NUCLEAR FACTOR KAPPA BETA AND THE INITIATION OF THE ATHEROSCLEROTIC LESIONP50HL056985 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI GIMBRONE, MICHAEL A · 1997 to 2006
$14.1M
Regulation of T Cell Responses in AtherosclerosisR01HL087282 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LICHTMAN, ANDREW H · 2007 to 2015
$4.0M
NHLBI NIH HHS P50 HL056985NHLBI NIH HHS P50HL56985.NHLBI NIH HHS R01 HL087282NHLBI NIH HHS R01HL087282
6 · The paper itself

Abstract

Myocardial inflammation and damage can lead to lethal acute or chronic cardiac failure. A variety of regulatory mechanisms limit the magnitude and duration of T cell responses in the heart. Insights into these regulatory mechanisms have come from studies of specific deficiencies in central or peripheral T cell tolerance which cause or enhance the severity of myocarditis. Under non-inflammatory conditions, constitutive DC presentation of cardiac peptides to naïve T cells in cardiac draining lymph nodes tolerizes recirculating naïve T cells specific for these antigens. Cardiac antigen-specific naïve T cells, especially those specific of α-myosin heavy chain peptides, become activated and differentiate into expanded clones of effector T cells under various conditions, such as cardiac infection and/or genetic variations in peripheral tolerance. The pathology that these effector cells cause in the myocardium is limited by PD-L1 expressed on myocardial cells in response to inflammatory cytokines, and by CTLA-4 dependent mechanisms. The PD-1:PD-L1 pathway works together with other control mechanisms to keep the heart safe from T cells, and combined impairment of this pathway along with other regulatory mechanisms synergize to cause myocarditis. T cell derived IFNγ contributes to the inflammatory damage to the heart in autoimmune myocarditis, but it also engages regulatory mechanisms that limit disease, including upregulation of PD-L1, and differentiation of TNF and iNOS expressing DCs from monocytes. iNOS derived from these DCs and other IFNγ stimulated cells inhibits expansion of T cells that cause myocarditis. Regulatory T cells also appear to be critical for suppression of effector T cells specific for myocardial antigens.

Indexed as

AnimalsAutoantigensB7-H1 AntigenCardiac MyosinsHeart FailureHumansImmune ToleranceInterferon-gammaMiceMyocarditisNitric Oxide Synthase Type IISignal TransductionT-LymphocytesAutoantigensB7-H1 AntigenCardiac MyosinsInterferon-gammaNitric Oxide Synthase Type IIAutoimmunityHeartMyocarditisMyosinT cellsTolerance

Identifiers

PMID23810579
PMCPMC3783609
OpenAlexW2150058408

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.