ArticleCell reports2017
Myocardial Infarction Primes Autoreactive T Cells through Activation of Dendritic Cells.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
93 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.
- Myocardial Immune Cells: The Basis of Cardiac Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023Pooled it
- Heart-specific T cell responses: from antigens to disease mechanisms.Nature reviews. Cardiology · 2026Review
- Dendritic Cells in the Immunoregulation of Myocardial Infarction: Mechanisms and Therapeutic Strategies.Cardiovascular drugs and therapy · 2026Review
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- Myocardial Immune Niches in Homeostasis and Inflammation.Immunological reviews · 2026Review
- T cells in acute and chronic myocarditis: from diagnosis to treatment.European heart journal · 2026Review
- T Cell Receptor Repertoires Across the Continuum of Vascular, Myocardial, and Age-Related Diseases.Immunological reviews · 2026Review
- Spatial and Functional Immune Profiling Identifies Impaired Vascular Repair in Human Myocardial Infarction.Biomedicines · 2026Article
- Myosin-Specific T Cells at the Heart of Myocardial Pathophysiology.JACC. Basic to translational science · 2026Article
- DNA-damaging chemotherapy reshapes cardiac-resident macrophage composition and function.Science immunology · 2026Article
- The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.Frontiers in immunology · 2026Review
- Immune Mechanisms in Myocardial Remodeling Following Myocardial Infarction: Focusing on Regulatory Networks of T Cell Responses.Journal of inflammation research · 2026Review
- Stem cell-derived extracellular vesicles as immunomodulators: a novel paradigm for post-myocardial infarction repair and regeneration.Frontiers in pharmacology · 2026Review
- Understanding immune checkpoint inhibitors-related myocarditis: Mechanisms and targeted therapeutic pathways.Theranostics · 2026Review
- Dendritic Cells: Origin, Classification, Development, Biological Functions, and Therapeutic Potential.MedComm · 2025Review
- CTLA-4-Ig therapy preserves cardiac function following myocardial infarction with reperfusion.Cardiovascular research · 2025Article
- B cells promote atrial fibrillation via autoantibodies.Nature cardiovascular research · 2025Article
- Sex differences in the chronic autoimmune response to myocardial infarction.Clinical science (London, England : 1979) · 2025Article
- Immune cell dynamics in heart failure: implicated mechanisms and therapeutic targets.ESC heart failure · 2025Review
- Mechanisms of mitochondrial damage-associated molecular patterns associated with inflammatory response in cardiovascular diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peripheral tolerance is crucial for avoiding activation of self-reactive T cells to tissue-restricted antigens. Sterile tissue injury can break peripheral tolerance, but it is unclear how autoreactive T cells get activated in response to self. An example of a sterile injury is myocardial infarction (MI). We hypothesized that tissue necrosis is an activator of dendritic cells (DCs), which control tolerance to self-antigens. DC subsets of a murine healthy heart consisted of IRF8-dependent conventional (c)DC1, IRF4-dependent cDC2, and monocyte-derived DCs. In steady state, cardiac self-antigen α-myosin was presented in the heart-draining mediastinal lymph node (mLN) by cDC1s, driving the proliferation of antigen-specific CD4
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What OpenQuestion holds
Registered trials
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.