- B.Sc., Simon Fraser University
- Ph.D., University of British Columbia
T Cell Biology
T cells are specialized cells of the immune system that protect host organisms from infection but that also contribute to a wide array of human diseases. Research in my laboratory is focused on understanding the mechanisms by which T cells become inappropriately activated in disease settings and how they cause organ damage. We have provided particular attention to how innate immune signals, such as cytokines secreted by innate immune cells and vascular cells, control the outcome of T cell responses. Within this context, processes that inhibit the activation of T cells are also being studied in order to potentially prevent disease-causing immune responses. Our studies on this topic are applied most directly to inflammatory vascular diseases, such as transplant arteriosclerosis and giant cell arteritis.
Nitric Oxide Signaling and Production
Nitric oxide (NO) is a bioactive gas that controls many cell biological responses. Dysregulation of its production and/or bioactivity is involved in many diseases. My laboratory is interested in understanding how NO effects cell signaling and how its production is controlled by NO synthases. We are specifically interested in how NO-mediated protein S-nitrosylation, a post-translational modification caused by NO, affects cell signaling pathways and cellular functions.
- von Rossum A et al. Bim regulates alloimmune-mediated vascular injury through effects on T cell activation and death. Arterioscler Thromb Vasc Biol 2014
- Lee M and Choy JC. Positive feedback regulation of human inducible nitric oxide synthase expression by Ras S-nitrosylation. J Biol Chem. 2013
- von Rossum et al. Inflammatory cytokines determine the susceptibility of human CD8 T cells to Fas-mediated activation-induced cell death through modulation of FasL and c-FLIP expression. J Biol Chem 2011
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