ArticleHypertension (Dallas, Tex. : 1979)2016
CD28/B7 Deficiency Attenuates Systolic Overload-Induced Congestive Heart Failure, Myocardial and Pulmonary Inflammation, and Activated T Cell Accumulation in the Heart and Lungs.
Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 53 citations in OpenAlex.
- Systolic pressure overload caused pulmonary oxidative stress, vessel remodeling and severe microvascular thrombosis in CD40 knockout mice through promoting platelet aggregation.Redox biology · 2026Article
- Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development.Redox biology · 2026Article
- CXCL10 Regulates Pressure Overload-Induced Heart Failure.JACC. Basic to translational science · 2026Article
- PHD2 Deletion in CD8Hypertension (Dallas, Tex. : 1979) · 2025Article
- Attenuation of myocardial ischemia-reperfusion injury in mice through CD80/86 deficiency: improved microvascular obstruction via reduced macrophage and T lymphocyte infiltration.Basic research in cardiology · 2025Article
- Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac inflammation and heart failure development.bioRxiv : the preprint server for biology · 2025Article
- IL-22 Attenuates Pressure Overload-Induced Heart Failure and Inflammation.Journal of cardiovascular translational research · 2025Article
- Article
- Pharmacological inhibition of IL12β is effective in treating pressure overload-induced cardiac inflammation and heart failure.Frontiers in immunology · 2025Article
- Genetic factors in the pathogenesis of cardio-oncology.Journal of translational medicine · 2024Review
- Immune checkpoints in cardiac physiology and pathology: therapeutic targets for heart failure.Nature reviews. Cardiology · 2024Review
- CD8 T cells promote heart failure progression in mice with preexisting left ventricular dysfunction.Frontiers in immunology · 2024Article
- Plasma metabolome mediates the causal relationship between immune cells and heart failure: a two-step bidirectional Mendelian randomization study.Frontiers in cardiovascular medicine · 2024Article
- Inhibition of NK1.1 signaling attenuates pressure overload-induced heart failure, and consequent pulmonary inflammation and remodeling.Frontiers in immunology · 2023Article
- Article
- Sodium-glucose Cotransporter 2 Inhibitors and Pathological Myocardial Hypertrophy.Current drug targets · 2023Article
- IL-12α deficiency attenuates pressure overload-induced cardiac inflammation, hypertrophy, dysfunction, and heart failure progression.Frontiers in immunology · 2023Article
- Understanding the Pathobiology of Pulmonary Hypertension Due to Left Heart Disease.Circulation research · 2022Review
- Isolevuglandin-Modified Cardiac Proteins Drive CD4+ T-Cell Activation in the Heart and Promote Cardiac Dysfunction.Circulation · 2021Article
- Does Transient Receptor Potential Vanilloid Type 1 Alleviate or Aggravate Pathological Myocardial Hypertrophy?Frontiers in pharmacology · 2021Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
The inflammatory response regulates congestive heart failure (CHF) development. T cell activation plays an important role in tissue inflammation. We postulate that CD28 or B7 deficiency inhibits T cell activation and attenuates CHF development by reducing systemic, cardiac, and pulmonary inflammation. We demonstrated that chronic pressure overload-induced end-stage CHF in mice is characterized by profound accumulation of activated effector T cells (CD3(+)CD44(high) cells) in the lungs and a mild but significant increase of these cells in the heart. In knockout mice lacking either CD28 or B7, there was a dramatic reduction in the accumulation of activated effector T cells in both hearts and lungs of mice under control conditions and after transverse aortic constriction. CD28 or B7 knockout significantly attenuated transverse aortic constriction-induced CHF development, as indicated by less increase of heart and lung weight and less reduction of left ventricle contractility. CD28 or B7 knockout also significantly reduced transverse aortic constriction-induced CD45(+) leukocyte, T cell, and macrophage infiltration in hearts and lungs, lowered proinflammatory cytokine expression (such as tumor necrosis factor-α and interleukin-1β) in lungs. Furthermore, CD28/B7 blockade by CTLA4-Ig treatment (250 μg/mouse every 3 days) attenuated transverse aortic constriction-induced T cell activation, left ventricle hypertrophy, and left ventricle dysfunction. Our data indicate that CD28/B7 deficiency inhibits activated effector T cell accumulation, reduces myocardial and pulmonary inflammation, and attenuates the development of CHF. Our findings suggest that strategies targeting T cell activation may be useful in treating CHF.
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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.