A5015597151- Viral Infections and Immunology Research
- Immune Cell Function and Interaction
- Atherosclerosis and Cardiovascular Diseases
- CAR-T cell therapy research
- Eosinophilic Disorders and Syndromes
- Cytokine Signaling Pathways and Interactions
- Mast cells and histamine
- Monoclonal and Polyclonal Antibodies Research
- Influenza Virus Research Studies
- Respiratory viral infections research
- IL-33, ST2, and ILC Pathways
- Eosinophilic Esophagitis
Johns Hopkins University
2023-2024
University of Washington
2016
Broadly neutralizing antibodies targeting a highly conserved region in the hemagglutinin (HA) stem protect against influenza infection. Here, we investigate protective efficacy of protein (HB36.6) computationally designed to bind with high affinity same HA stem. We show that intranasal delivery HB36.6 affords protection mice lethally challenged diverse strains independent Fc-mediated effector functions or host antiviral immune response. This prevents infection when given as single dose 6.0...
Cardiac myosin-specific (MyHC) T cells drive the disease pathogenesis of immune checkpoint inhibitor–associated myocarditis (ICI-myocarditis). To determine whether MyHC are tissue-resident memory (T RM ) cells, we characterized cardiac in naive mice and established that they have a distinct phenotypic transcriptional profile can be defined by their upregulation CD69, PD-1, CXCR6. We then investigated effects injury through modified experimental autoimmune mouse model an ischemia–reperfusion...
Hypereosinophilic syndrome is a progressive disease with extensive eosinophilia that results in organ damage. Cardiac pathologies are the main reason for its high mortality rate. A better understanding of mechanisms eosinophil-mediated tissue damage would benefit therapeutic development. Here, we describe cardiac developed mouse model hypereosinophilic syndrome. These IL-5 transgenic mice exhibited decreased left ventricular function at young age which worsened age. Mechanistically,...
Currently, there are no therapies targeting specific pathogenic pathways in myocarditis. IL (interleukin)-1 blockade has shown promise preclinical studies and case reports. We hypothesized that of IL1RAP (IL-1 receptor accessory protein), a shared subunit the IL-1, IL-33, IL-36 receptors, could be more efficient than IL-1 alone.
Abstract IL-1, IL-33 and IL-36 have complementary pro-inflammatory roles during the immune response promoting autoimmune inflammatory diseases, such as myocarditis. Therapeutic blockers targeting IL-1 pathway previously been developed. However, we hypothesized that blockade of shared co-receptor these three pathways, receptor accessory protein (IL1RAP), would exhibit a more potent broader anti-inflammatory profile. To investigate this hypothesis, induced coxsackievirus B3 (CVB3)-mediated or...