Immunology and Infectious Disease Researchers
Adam Hoppe
The focus of my lab is to understand how macrophages contribute to immune responses, including antibody-mediated killing of cancerous and infected host cells. We develop used new live-cell and high-throughput imaging methods to analyze receptor signaling and cell biological events that regulate these processes. Additionally, we develop and apply whole-genome screening methods based on CRISPR to identify biochemical pathways that regulate macrophage effector function. Our current work is focused on the immune/cytokine regulation of Fc-gamma receptor mediated killing by therapeutic antibodies and identifying host genes that contribute or inhibit entry of SARS-CoV-2.
Rachel Willand-Charnley
The overall objective of the Willand-Charnley Lab is to generate interdisciplinary solutions to biological problems facing society synergistically through the lab鈥檚 organic chemistry and glyco-cancer immunology research programs. The group鈥檚 glyco-cancer immunology investigations inform synthetic targets for glycan therapeutics producing innovative synthetic methods and materials to evaluate their effectiveness against important cancers. The labs intersection of organic chemistry and biology allows the unique advantage of identifying promising therapeutic targets, synthesis of therapeutics in house and testing of their effectiveness.
The Savinov Lab focuses on studying the underlying mechanisms controlling organ-specific autoimmune diseases such as type I diabetes (T1D). Progression of T1D involves the activation of autoimmune T cells, consequent homing of activated lymphocytes to the pancreatic islets, and ensuing destruction of insulin-producing beta cells. The Savinov Lab current research projects are focused on the mechanisms involved in the regulation of T cell activation and tolerance in regard to T1D, even though most of them could take place in other autoimmune processes. Using genetic mouse models, and variety of primary and established cell lines, we are examining the molecular mechanisms leading to inefficient negative co-stimulation, a control mechanism for T cell activation by auto-antigens, along with some defects in the intracellular signaling cascades involved in the autoimmune process.
