ArticleNature communications2017
T cell costimulation blockade blunts pressure overload-induced heart failure.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 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
137 citing papers in PubMed, 1 synthesis or guideline pooled it, 191 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
- Cytomegalovirus Latency Fuels Inflammation Following Myocardial Infarction.Circulation research · 2026Article
- Integrative Omics Analysis Reveals a CD206Barrier immunity · 2026Article
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- Therapeutic Applications of Immunobiologics in Autoimmune and Inflammatory Diseases.Pharmaceutics · 2026Review
- Inhibition of the programmed death protein 1 immune checkpoint and the development of heart failure in the presence of prior cardiac ischaemia.Cardiovascular research · 2026Article
- Targeting Lymph Node Entry to Improve Cardiac Graft Tolerance.Circulation · 2026Article
- T Cell Receptor Repertoires Across the Continuum of Vascular, Myocardial, and Age-Related Diseases.Immunological reviews · 2026Review
- Review
- CXCL10 Regulates Pressure Overload-Induced Heart Failure.JACC. Basic to translational science · 2026Article
- T Cell Polarization in Heart Failure: Any Flavor, as Long as It Is Th1.JACC. Basic to translational science · 2026Article
- Targeting immunometabolic pathways with AZD1656 alleviates inflammation and metabolic dysfunction in type 2 diabetic cardiomyopathy.Nature cardiovascular research · 2026Article
- Alpha-7 nicotinic acetylcholine receptor: targeting the interplay between inflammation, renin-angiotensin aldosterone system, and nervous system for the novel treatment of heart failure.Frontiers in pharmacology · 2026Review
- B lymphocytes contribute Angiotensin II induced cardiac hypertrophy.Scientific reports · 2025Article
- Role of NPPB for recovery post ventricular assist device in paediatric dilated cardiomyopathy: Single-cell multiomics.ESC heart failure · 2025Article
- Cardioimmunologic response patterns after an acute heart failure event: Design and first results of AHF-ImmunoCS.ESC heart failure · 2025Article
- CTLA-4-Ig therapy preserves cardiac function following myocardial infarction with reperfusion.Cardiovascular research · 2025Article
- Circulating CD19 B cell count, myocardial injury and clinical outcomes in patients with heart failure.ESC heart failure · 2025Article
- Heart failure-specific cardiac fibroblasts contribute to cardiac dysfunction via the MYC-CXCL1-CXCR2 axis.Nature cardiovascular research · 2025Article
77 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
18 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure (HF) is a leading cause of mortality. Inflammation is implicated in HF, yet clinical trials targeting pro-inflammatory cytokines in HF were unsuccessful, possibly due to redundant functions of individual cytokines. Searching for better cardiac inflammation targets, here we link T cells with HF development in a mouse model of pathological cardiac hypertrophy and in human HF patients. T cell costimulation blockade, through FDA-approved rheumatoid arthritis drug abatacept, leads to highly significant delay in progression and decreased severity of cardiac dysfunction in the mouse HF model. The therapeutic effect occurs via inhibition of activation and cardiac infiltration of T cells and macrophages, leading to reduced cardiomyocyte death. Abatacept treatment also induces production of anti-inflammatory cytokine interleukin-10 (IL-10). IL-10-deficient mice are refractive to treatment, while protection could be rescued by transfer of IL-10-sufficient B cells. These results suggest that T cell costimulation blockade might be therapeutically exploited to treat HF.
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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.