A5021871255- Cardiac Fibrosis and Remodeling
- T-cell and B-cell Immunology
- Atherosclerosis and Cardiovascular Diseases
- CAR-T cell therapy research
- Immune Response and Inflammation
- Immunotherapy and Immune Responses
- Receptor Mechanisms and Signaling
- Peptidase Inhibition and Analysis
- Viral Infections and Immunology Research
- Immune Cell Function and Interaction
- Acute Myocardial Infarction Research
- Adipokines, Inflammation, and Metabolic Diseases
- Cardiovascular Effects of Exercise
- Herpesvirus Infections and Treatments
- Antiplatelet Therapy and Cardiovascular Diseases
- Fibromyalgia and Chronic Fatigue Syndrome Research
- Inflammasome and immune disorders
- Sports injuries and prevention
- Signaling Pathways in Disease
- Protease and Inhibitor Mechanisms
- Single-cell and spatial transcriptomics
- Cardiac Structural Anomalies and Repair
- Cytomegalovirus and herpesvirus research
- Health, psychology, and well-being
- Tissue Engineering and Regenerative Medicine
Universitätsklinikum Würzburg
2021-2025
Institute of Virology of the Slovak Academy of Sciences
2020
University of Würzburg
2017-2018
In the past years, several studies investigated how distinct immune cell subsets affects post-myocardial infarction repair. However, whether and tissue environment controls these local responses has remained poorly understood. We sought to investigate antigen-specific T-helper cells differentiate under myocardial milieu's influence.
Abstract Aims Recent studies have revealed that B cells and antibodies can influence inflammation remodelling following a myocardial infarction (MI) culminating in heart failure—but the mechanisms underlying these observations remain elusive. We therefore conducted mice deep phenotyping of post-MI B-cell responses infarcted hearts mediastinal lymph nodes, which drain myocardium. Thereby, we sought to dissect controlling mobilization activity situ. Methods results Histological, flow...
Aging entails profound immunological transformations that can impact myocardial homeostasis and predispose to heart failure. However, preclinical research in the immune-cardiology field is mostly conducted young healthy animals, which potentially weakens its translational relevance. Herein, we sought investigate how aging T-cell compartment associates with changes cell biology aged mice.We phenotyped antigen-experienced effector/memory T cells purified from heart-draining lymph nodes of 2-,...
Success of DC vaccines relies on the quality antigen presentation, costimulation, lymph node migration, and release IL-12, in case Th1 priming. Here, we provide evidence for interaction between injected vaccine DCs with endogenous node-resident induction. While migration was essential delivery to node, contributed only partially Th0 priming were unable instruct generation. Instead, that XCR1+ are activated by present cognate IL-12 polarization. The timing interactions draining nodes appeared...
Abstract Platelet activation plays a critical role in thrombosis. Inhibition of platelet is cornerstone treatment acute organ ischemia. ACKR3 surface expression independently associated with all-cause mortality CAD patients. In novel genetic mouse strain, we show that megakaryocyte/platelet-specific deletion results enhanced and thrombosis vitro vivo. Further, performed ischemia/reperfusion experiments (transient LAD-ligation tMCAO) mice to assess the impact deficiency platelets on tissue...
Background Arrhythmogenic cardiomyopathy (ACM) is a genetic heart muscle disease, which presents with arrhythmias and sudden cardiac death, along progressive remodeling myocardial inflammation. This study aims to elucidate the patterns of [ 18 F]‐fluorodeoxyglucose ([ F]‐FDG) uptake in mouse model plakoglobin‐associated disease better understand its diagnostic potential. Methods Results Plakoglobin ( Jup ) knockout mice developed that presented an ACM‐like phenotype at 6 weeks age. Flow...
The cardiovascular and immune systems undergo profound intertwined alterations with aging. Recent studies have reported that an accumulation of memory terminally differentiated T cells in elderly subjects can fuel myocardial aging boost the progression heart diseases. Nevertheless, it remains unclear whether immunological senescence profile is sufficient to cause age-related cardiac deterioration or merely acts as amplifier previous tissue-intrinsic damage. Herein, we sought decompose...
Mounting experimental and clinical evidence has revealed that adaptive immune mechanisms targeting myocardial antigens are triggered by different forms of cardiac injury impact disease progression. B T lymphocytes recognize specific via unique receptors generated through a somatic rearrangement process generates potential repertoire 10
Irreversible fibrosis is a hallmark of myocardial infarction (MI) and heart failure. Extracellular matrix protein-1 (ECM-1) up-regulated in these hearts, localized to fibrotic, inflammatory, perivascular areas. ECM-1 originates predominantly from fibroblasts, macrophages, pericytes/vascular cells uninjured human mouse M1 M2 macrophages myofibroblasts after MI. stimulates fibroblast-to-myofibroblast transition, up-regulates key fibrotic inflammatory pathways, inhibits cardiac fibroblast...
Immature or semi-mature dendritic cells (DCs) represent tolerogenic maturation stages that can convert naive T into Foxp3+ induced regulatory (iTreg). Here we found murine bone marrow-derived DCs (BM-DCs) treated with cholera toxin (CT) matured by up-regulating MHC-II and costimulatory molecules using either high low doses of CT (CThi, CTlo) cAMP, a known mediator signals. However, all three conditions also mRNA both isoforms the molecule cytotoxic lymphocyte antigen 2 (CTLA-2α CTLA-2β)....
Summary Heart-specific T cells play important roles in myocardial diseases, including myocarditis, infarction, and heart failure. However, only few cardiac antigens their respective specific cell receptors (TCRs) have been validated so far. Therefore, we sought to identify new epitopes C57BL/6 mice characterize the TCRs. Antigen mapping of myosin heavy chain alpha (MYHCA) led identification a 9-mer epitope (MYHCA 724-732 ) recognized by CD8 + cells. Single-cell TCR sequencing (scTCR-seq)...
Abstract Myocardial infarction (MI) is associated with an inflammatory process mainly attributed to innate immune components. Very recently, the role of T-cells in both inflammation and healing has been suggested through various human mouse studies. Previous studies showed that CD4+ CD8+ T cells affect post-MI repair but did not investigate how leverage cell biology predict outcomes patients. For instance, antigenic trigger still unknown human. Indeed, others we identified T-cell specific...
Abstract Background Myocardial infarction (MI) is a sterile inflammatory condition associated with tissue injury that results in the activation of T helper cell targeting cardiac antigens. However, differentiation trajectories and situ activity heart-specific CD4 + cells activated MI context remain poorly understood. Methods Herein, we combined T-cell receptor transgenic models myocardial protein, single-cell transcriptomics, functional phenotyping to elucidate how myosin-specific (TCR-M)...