ArticlePloS one2012
Reciprocal interaction between macrophages and T cells stimulates IFN-γ and MCP-1 production in Ang II-induced cardiac inflammation and fibrosis.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 94 citations in OpenAlex.
- Small-molecule LF3 alleviates angiotensin II-induced cardiac dysfunction via attenuating cardiac fibrosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The role of macrophages in cardiac diseases: a review of the origins, functional diversity, and therapeutic potential.Frontiers in immunology · 2026Review
- Macrophage Polarization Profiling in Dynamic Culture System.Cellular and molecular bioengineering · 2025Article
- NADPH Oxidases in Cancer Therapy-Induced Cardiotoxicity: Mechanisms and Therapeutic Approaches.Cardiovascular toxicology · 2025Review
- Cardiac Fibroblastic Niches in Homeostasis and Inflammation.Circulation research · 2024Review
- Macrophages coordinate immune response to laser-induced injury via extracellular traps.Journal of neuroinflammation · 2024Article
- Interferons and interferon-related pathways in heart disease.Frontiers in cardiovascular medicine · 2024Review
- The relationship between inflammatory factors and heart failure: evidence based on bidirectional Mendelian randomization analysis.Frontiers in cardiovascular medicine · 2024Article
- A digital nanoplasmonic microarray immunosensor for multiplexed cytokine monitoring during CAR T-cell therapy from a leukemia tumor microenvironment model.Biosensors & bioelectronics · 2023Article
- Inhibition of NK1.1 signaling attenuates pressure overload-induced heart failure, and consequent pulmonary inflammation and remodeling.Frontiers in immunology · 2023Article
- Roles of peripheral immune cells in the recovery of neurological function after ischemic stroke.Frontiers in cellular neuroscience · 2022Review
- Estrogenic bias in T-Lymphocyte biology: Implications for cardiovascular disease.Pharmacological research · 2021Review
- Finding Solutions for Fibrosis: Understanding the Innate Mechanisms Used by Super-Regenerator Vertebrates to Combat Scarring.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Review
- Sialomucin CD43 Plays a Deleterious Role in the Development of Experimental Heart Failure Induced by Pressure Overload by Modulating Cardiac Inflammation and Fibrosis.Frontiers in physiology · 2021Article
- Adding insult to injury - Inflammation at the heart of cardiac fibrosis.Cellular signalling · 2021Review
- Inflammatory responses mediate brain-heart interaction after ischemic stroke in adult mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Rejection of xenogeneic porcine islets in humanized mice is characterized by graft-infiltrating Th17 cells and activated B cells.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020Article
- New Approaches to Target Inflammation in Heart Failure: Harnessing Insights from Studies of Immune Cell Diversity.Annual review of physiology · 2020Review
- The Dynamic Interplay Between Cardiac Inflammation and Fibrosis.Frontiers in physiology · 2020Review
- CD8American journal of physiology. Heart and circulatory physiology · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe inflammatory response plays a critical role in hypertension-induced cardiac remodeling. We aimed to study how interaction among inflammatory cells causes inflammatory responses in the process of hypertensive cardiac fibrosis. METHODOLOGY/PRINCIPAL
findingsInfusion of angiotensin II (Ang II, 1500 ng/kg/min) in mice rapidly induced the expression of interferon γ (IFN-γ) and leukocytes infiltration into the heart. To determine the role of IFN-γ on cardiac inflammation and remodeling, both wild-type (WT) and IFN-γ-knockout (KO) mice were infused Ang II for 7 days, and were found an equal blood pressure increase. However, knockout of IFN-γ prevented Ang II-induced: 1) infiltration of macrophages and T cells into cardiac tissue; 2) expression of tumor necrosis factor α and monocyte chemoattractant protein 1 (MCP-1), and 3) cardiac fibrosis, including the expression of α-smooth muscle actin and collagen I (all p<0.05). Cultured T cells or macrophages alone expressed very low level of IFN-γ, however, co-culture of T cells and macrophages increased IFN-γ expression by 19.8±0.95 folds (vs. WT macrophage, p<0.001) and 20.9 ± 2.09 folds (vs. WT T cells, p<0.001). In vitro co-culture studies using T cells and macrophages from WT or IFN-γ KO mice demonstrated that T cells were primary source for IFN-γ production. Co-culture of WT macrophages with WT T cells, but not with IFN-γ-knockout T cells, increased IFN-γ production (p<0.01). Moreover, IFN-γ produced by T cells amplified MCP-1 expression in macrophages and stimulated macrophage migration. CONCLUSIONS/SIGNIFICANCE: Reciprocal interaction between macrophages and T cells in heart stimulates IFN-γ expression, leading to increased MCP-1 expression in macrophages, which results a forward-feed recruitment of macrophages, thus contributing to Ang II-induced cardiac inflammation and fibrosis.
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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.