A5018359516- Immune Cell Function and Interaction
- Immunotherapy and Immune Responses
- T-cell and B-cell Immunology
- CAR-T cell therapy research
- Immune Response and Inflammation
- IL-33, ST2, and ILC Pathways
- Chemical Synthesis and Analysis
- Synthesis and Biological Evaluation
- Nuclear Receptors and Signaling
University of Cincinnati
2019-2023
Cincinnati Children's Hospital Medical Center
2019-2022
University of Cincinnati Medical Center
2017
Northwestern University
2010-2013
The University of Texas Southwestern Medical Center
2010
Midwestern University
2010
Abstract Most effector CD8 + T cells die, while some persist and become either “effector” (T EM ) or “central” CM memory cells. Paradoxically, with greater potential have higher levels of the pro-apoptotic molecule Bim. Here, we report, using a novel Bim-mCherry knock-in mouse, that high Bim preferentially develop into remained stable were regulated by DNA methylation at promoter. Notably, Bcl-2 required for hi to survive. Using Nur77-GFP mice as an indicator TCR signal strength, Nur77...
Abstract The precursors of TCRαβ+CD8αα+ intraepithelial lymphocytes (IEL) arise in the thymus through a complex process agonist selection. We and others have shown that proapoptotic protein, Bim, is critical to limit number thymic IEL (IELp), as loss Bim at CD4+CD8+ double-positive stage development drastically increases IELp. factors determining this cell death versus survival decision remain largely unknown. In study, we used CD4CreBcl2f/f mice define role antiapoptotic protein Bcl-2...
Abstract Following their proliferative expansion and differentiation into effector cells like Th1, Tfh, T central memory precursors (Tcmp), most CD4+ die, while some survive become cells. Here, we explored how Bcl-2 family members controlled the survival of during distinct phases mouse acute LCMV infection. During expansion, found that Th1 dominated response, downregulated expression Bcl-2, did not require for survival. Instead, they relied on anti-apoptotic protein, A1 Similarly, Th17 in an...
Abstract The mouse MHC Ib molecule Qa-1b plays roles in both antigen presentation and immune regulation different disease models. Further, the human homologue of Qa-1b, HLA-E, can present Mycobacterium tuberculosis (Mtb) peptides to CD8+ T cells. In viral infections, suppresses NK cell function by interacting with inhibitory CD94/NKG2A molecules. addition, activate regulatory cells, which suppress CD4+ responses EAE. However, role infection is unknown. this study, we find expression...
Abstract The murine MHC Ib molecule Qa-1b is known to play roles in both antigen presentation during infection by intracellular pathogens, as well an immunoregulatory role autoimmune and viral disease models. It has been shown that able suppress NK cell CD8+ T activity through the interaction of /self-peptide complexes with inhibitory CD94/NKG2A molecules on activated effector cells. We find expression upregulated a variety types mouse model low-dose, aerogenic Mycobacterium tuberculosis...
Abstract Unlike other MHC molecules, the CD1 family presents self and foreign lipid antigens to multiple T cell subsets. In humans, this consists of group 1 molecules CD1a, b c 2 molecule CD1d. While CD1d-restricted NKT cells have been well-studied, our knowledge development function CD1-restricted has limited by lack a suitable animal model. We generated double transgenic mice (hCD1Tg/HJ1Tg) that express human proteins in pattern similar observed humans addition TCR from CD1b-restricted...