A5101653843- Viral Infections and Immunology Research
- Cardiac Fibrosis and Remodeling
- IL-33, ST2, and ILC Pathways
- Immune Cell Function and Interaction
- Medical Imaging Techniques and Applications
- Eosinophilic Esophagitis
- Cardiac Structural Anomalies and Repair
- Eosinophilic Disorders and Syndromes
- Radiomics and Machine Learning in Medical Imaging
- Whipple's Disease and Interleukins
- Medical Imaging and Pathology Studies
- Radiopharmaceutical Chemistry and Applications
- Phytochemistry and biological activity of medicinal plants
- Lung Cancer Diagnosis and Treatment
- Traditional Chinese Medicine Analysis
- Cellular transport and secretion
- Protein Kinase Regulation and GTPase Signaling
- Cancer, Hypoxia, and Metabolism
- Cardiovascular Effects of Exercise
- T-cell and B-cell Immunology
- Flavonoids in Medical Research
- Phagocytosis and Immune Regulation
- Complement system in diseases
- Signaling Pathways in Disease
Johns Hopkins Medicine
2016-2020
Johns Hopkins University
2016-2020
University of Baltimore
2017
Jiangyin People's Hospital
2013
National University of Singapore
2011-2012
Fujian Provincial Hospital
2010
Fujian Medical University
2010
Cardiac manifestations are a major cause of morbidity and mortality in patients with eosinophil-associated diseases. Eosinophils thought to play pathogenic role myocarditis. We investigated the pathways that recruit eosinophils heart using model eosinophilic myocarditis, which experimental autoimmune myocarditis (EAM) is induced IFNγ-/- IL-17A-/- mice. Two conditions necessary for efficient eosinophil trafficking heart: high eotaxin (CCL11, CCL24) expression receptor CCR3 by eosinophils....
Two types of monocytes, Ly6Chi and Ly6Clo, infiltrate the heart in murine experimental autoimmune myocarditis (EAM). We discovered a role for cardiac fibroblasts facilitating monocyte-to-macrophage differentiation both Ly6Clo cells, allowing these macrophages to perform divergent functions progression. During acute phase EAM, IL-17A is highly abundant. It signals through attenuate efferocytosis monocyte-derived (MDMs) simultaneously prevents differentiation. demonstrated an inverse clinical...
The causative effect of GM-CSF produced by cardiac fibroblasts to development heart failure has not been shown. We identified the pathological GM-CSF-producing fibroblast subset and specific deletion IL-17A signaling these cells attenuated inflammation failure. describe here CD45- CD31- CD29+ mEF-SK4+ PDGFRα+ Sca-1+ periostin+ (Sca-1+ ) as main producer in both experimental autoimmune myocarditis myocardial infarction mouse models. Specific ablation (PostnCre Il17rafl/fl protected mice from...
Hereditary homozygous C1q deficiency is rare, but it almost certainly causes systemic lupus erythematosus. On the other hand, levels can decline in erythematosus patients without apparent gene defects and versatility production a likely cause. As an 18-subunit protein, assembled 1:1:1 ratio from three different subunits. The human genes are closely bundled on chromosome 1 (C1qA-C1qC-C1qB) their basal IFNγ-stimulated expression, largely restricted to macrophages dendritic cells, apparently...
Innate lymphoid cells (ILC) are a subset of leukocytes with properties that lack antigen specific receptors. They can be stimulated by and exert their effect via cytokine axes, whereas Natural Killers (NK) the only known cytotoxic member this family. ILCs considered key in linking innate adaptive response physiologic pathologic environments. In study, we investigated non-cytotoxic cardiac physiologic, inflammatory, ischemic conditions. We found healthy humans mice, predominantly type...
We find that cardiac group 2 innate lymphoid cells (ILC2s) are essential for the development of IL-33-induced eosinophilic pericarditis. show a pathogenic role ILC2s in inflammation, which activated by IL-33 drive pericarditis collaboration with fibroblasts. ILCs, not T and B cells, required transferred to heart Rag2−/−Il2rg−/− mice restore their susceptibility eosinophil infiltration. Moreover, direct fibroblasts produce eotaxin-1. also eosinophils reside mediastinal cavity...
Two types of monocytes, Ly6Chi and Ly6Clo, infiltrate the heart in murine experimental autoimmune myocarditis (EAM). We discovered a previously unappreciated role for cardiac fibroblasts facilitating both Ly6Clo monocyte-to-macrophage differentiation, allowing these macrophages to perform divergent functions progression. During acute phase EAM, IL-17A is highly abundant. It signals through attenuate efferocytosis monocyte-derived simultaneously prevents differentiation. demonstrated an...
Abstract Heart diseases are the leading causes of mortality and morbidity worldwide. The post-injury cardiac inflammation remodeling process determined severity damage likelihood developing heart failure. We have adapted both experimental autoimmune myocarditis (EAM) myocardial infarction (MI) mouse model to investigate mechanism behind remodeling. showed that Interleukin 17 (IL-17A) signaling is required for adverse fibrosis in EAM MI models. IL-17A induces fibroblast (CF) produce...