A5101677195- Immune Cell Function and Interaction
- Viral Infections and Immunology Research
- CAR-T cell therapy research
- Cancer Immunotherapy and Biomarkers
- Sarcoidosis and Beryllium Toxicity Research
- Immune cells in cancer
- Antifungal resistance and susceptibility
- IL-33, ST2, and ILC Pathways
- Mast cells and histamine
- Extracellular vesicles in disease
- Eosinophilic Esophagitis
- Eosinophilic Disorders and Syndromes
- Malaria Research and Control
- Drug Transport and Resistance Mechanisms
- Atherosclerosis and Cardiovascular Diseases
- HIV Research and Treatment
- Peptidase Inhibition and Analysis
- Cytokine Signaling Pathways and Interactions
Johns Hopkins University
2023-2024
Johns Hopkins Medicine
2023
Immune checkpoint inhibitors (ICIs) are specialized monoclonal antibodies (mAbs) that target immune checkpoints and their ligands, counteracting cancer cell-induced T-cell suppression. Approved ICIs like cytotoxic T-lymphocyte antigen-4 (CTLA-4), programmed death-1 (PD-1), its ligand PD-L1, lymphocyte activation gene-3 (LAG-3) have improved patient outcomes by enhancing anti-tumor responses. However, some patients unresponsive, others experience immune-related adverse events (irAEs),...
Objective Arthritis associated with immune checkpoint inhibitor therapies highlights the importance of expression for joint homeostasis. We investigated role programmed death ligand (PD‐L) 1 in synovium using a collagen‐induced arthritis (CIA) mouse model. Methods blocked PD‐L1 blocking antibodies during CIA and assessed severity by clinical histologic scoring. origin synovial macrophages were flow cytometry parabiosis. used Cre‐Lox mice to ascertain protective PD‐L1–expressing arthritis....
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,...
Hemozoin is a crystal synthesized by Plasmodium parasites during hemoglobin digestion in the erythrocytic stage. The hemozoin released when egress from red blood cell, which complexed with parasite DNA, cleared circulation circulating and tissue-resident monocytes macrophages, respectively. Recently, we reported that intravenous administration of purified berghei DNA (HzPbDNA) resulted an innate immune response blocked liver stage development sporozoites was dose-dependent time-limited....
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...