CD4+ T-lymphocytes exhibit biphasic kinetics post-myocardial infarction

Article Cardiac & Cardiovascular Systems

Estrogen Receptor-β Agonists Modulate T-Lymphocyte Activation and Ameliorate Left Ventricular Remodeling During Chronic Heart Failure

Rachel Rosenzweig et al.

Summary: The study identified the activation of ER-alpha signaling in CD4(+) T cells during ischemic heart failure and demonstrated the potential of using ER beta agonist OSU-ERb-012 to inhibit T cells and reduce left ventricular remodeling. Treatment with OSU-ERb-012 effectively inhibited proliferation and proinflammatory cytokine expression in T cells, leading to improved cardiac outcomes in a mouse model.

CIRCULATION-HEART FAILURE (2022)

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Article Cardiac & Cardiovascular Systems

TNFR1 Contributes to Activation-Induced Cell Death of Pathological CD4+T Lymphocytes During Ischemic Heart Failure

Vinay Kumar et al.

Summary: CD4+ T cells become pathological during heart failure, and the expression of tumor necrosis factor alpha (TNF-α) and tumor necrosis factor receptor 1 (TNFR1) increases in these activated cells. The study shows that TNFR1 plays a crucial role in suppressing prosurvival and proliferative signals in CD4+ T cells during heart failure, without altering their pathological activity.

JACC-BASIC TO TRANSLATIONAL SCIENCE (2022)

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Article Cardiac & Cardiovascular Systems

Isolevuglandin-Modified Cardiac Proteins Drive CD4+T-Cell Activation in the Heart and Promote Cardiac Dysfunction

Njabulo Ngwenyama et al.

Summary: The study found that TCR antigen recognition increases in the left ventricle as cardiac dysfunction progresses, with a limited repertoire of activated CD4+ T-cell clonotypes identified in the left ventricle. Antigen presentation of endogenous antigens was necessary for the development of cardiac dysfunction, and scavenging IsoLGs reduced TCR activation and prevented cardiac dysfunction. This highlights the important role of reactive oxygen species-induced formation of IsoLG-modified cardiac neoantigens in TCR-dependent CD4+ T-cell activation within the heart.

CIRCULATION (2021)

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Article Multidisciplinary Sciences

Cytotoxic CD8+ T cells promote granzyme B-dependent adverse post-ischemic cardiac remodeling

Icia Santos-Zas et al.

Summary: This study reveals the detrimental role of CD8(+) T lymphocytes following acute myocardial infarction, showing that they release Granzyme B in the ischemic heart tissue leading to cardiomyocyte apoptosis, adverse ventricular remodeling, and deterioration of myocardial function. Depletion of CD8(+) T lymphocytes leads to reduced apoptosis, inhibited inflammatory response, limited myocardial injury, and improved heart function. Elevated circulating levels of GRANZYME B in AMI patients may predict increased risk of death at 1-year follow-up. Targeting pathogenic CD8(+) T lymphocytes could be a potential therapeutic strategy in the setting of acute myocardial infarction.

NATURE COMMUNICATIONS (2021)

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Article Cardiac & Cardiovascular Systems