A5068088148- Viral Infections and Immunology Research
- Whipple's Disease and Interleukins
- Eosinophilic Disorders and Syndromes
- Cytomegalovirus and herpesvirus research
- IL-33, ST2, and ILC Pathways
- Cytokine Signaling Pathways and Interactions
- Respiratory viral infections research
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
Pfizer (United States)
2025
Abbott (United States)
2015
Bloomberg (United States)
2015
Johns Hopkins University
2013
Abstract Immune checkpoint inhibitors have shown limited success in breast cancer, the most common and deadly cancer women worldwide. Novel immune therapies like CD3 engaging bispecific antibodies clinical promise hematologic malignancies. However, developing bispecifics for solid tumors has been challenging due to difficulty identifying tumor-specific antigens. B7-H4 is proposed as an attractive tumor-associated antigen therapeutics with comprehensive coverage regardless of molecular...
Abstract Inflammatory dilated cardiomyopathy (DCMi) is a major cause of heart failure in children and young adults, patients often require transplant. DCMi develops up to 30% myocarditis patients, but the mechanisms involved disease progression are poorly understood. In wildtype (WT) BALB/cJ mice, experimental autoimmune (EAM) progresses with failure. Surprisingly, eosinophil-deficient ΔGATA1 mice developed similar WT were completely protected from DCMi. This indicates that eosinophils...
Abstract Myocarditis is the inflammation of cardiac muscle and among leading causes sudden failure in young adults. We demonstrate here that natural killer (NK) cells, a subset Type I innate lymphoid cell (ILC) group, suppress experimental autoimmune myocarditis (EAM). EAM was initiated BALB/c mice by immunization with myocarditogenic peptide emulsified complete Freund's adjuvant. During disease, activated NK cells accumulated heart, secreted interferonγ, perforin, granzyme-B, expressed...
Abstract Using a model of experimental autoimmune myocarditis (EAM), we established the requirement IL-23 for induction cardiac autoimmunity, as Il23a-/- mice failed to mount an efficient Th17 response after immunization and were protected from myocarditis. Furthermore, discovered that has divergent effects on CD4+ T cell pathogenicity IL-17A production. First, switches in cells, but becomes dispensable once autoreactivity is already established: cells raised WT donors able induce EAM...
Abstract Deviation to autoaggressive T helper 17 (Th17) responses has been reported account for the protective effect of interferon-gamma (IFNγ) in certain animal models autoimmune disease. Building on our previous findings that interleukin-17 (IL17) signaling is critical progression experimental myocarditis (EAM) dilative heart failure, we sought address question whether IL17 mediated severe form EAM observed IFNγ-deficient mice. To surprise, found IFNγ-/-IL17A-/- double-knockout (DKO) mice...