- Immune Cell Function and Interaction
- T-cell and B-cell Immunology
- Immune Response and Inflammation
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- CAR-T cell therapy research
- Neurological Disorders and Treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- IL-33, ST2, and ILC Pathways
- Clostridium difficile and Clostridium perfringens research
- Alzheimer's disease research and treatments
- Amoebic Infections and Treatments
- Parkinson's Disease Mechanisms and Treatments
- Parasitic Infections and Diagnostics
University of Alabama at Birmingham
2023-2024
Washington University in St. Louis
2019-2022
Both higher- and lower-affinity self-reactive CD4+ T cells are expanded in autoimmunity; however, their individual contribution to disease remains unclear. We addressed this question using peptide-MHCII chimeric antigen receptor (pMHCII-CAR) specifically deplete peptide-reactive mice. Integration of improvements CAR engineering with TCR repertoire analysis was critical for interrogating vivo the role affinity autoimmunity. Our original MOG35-55 pMHCII-CAR, which targeted only higher-affinity...
The success of B cell depletion therapies and identification leptomeningeal ectopic lymphoid tissue (ELT) in patients with multiple sclerosis (MS) has renewed interest the antibody-independent pathogenic functions cells during neuroinflammation. timing location antigen presentation MS its animal model experimental autoimmune encephalomyelitis (EAE) remain undefined. Using a new EAE system that incorporates temporal regulation MHCII expression by myelin-specific cells, we observed rapid...
Abstract Lewy pathology due to alpha-synuclein (α-syn) inclusions is one of the major hallmarks Parkinson’s Disease (PD). β-Amyloid (Aβ) and phosphorylated-tau, pathologies usually found in Alzheimer’s (AD), have also been implicated PD, with over 50% patients exhibited co-expression these proteins (co-pathologies). In both AD PD postmortem tissue, neuroinflammation – activation microglia resident macrophages infiltration immune cells from periphery, including T monocytes–are drivers...
Abstract Maintenance of immune homeostasis to the intestinal mictrobiota is dependent on a population effector regulatory T (eTreg) cells that develop from microbiota-reactive induced (i)Treg cells. A cardinal feature eTreg their production IL-10, which plays non-redundant role in tolerance commensal microbes. Here, we identify an unexpected for IL-2-induced Stat3 signaling program iTreg cell differentiation and Il10 transcriptional competency. IL-2 proved be both necessary sufficient...