Office: 302A Rowell
Dr. Eyal Amiel received his Ph.D. in Microbiology and Immunology from the Geisel School of Medicine at Dartmouth College. He performed his postdoctoral training at the Trudeau Institute in Saranac Lake, NY prior to joining the faculty of the Department of Medical Laboratory and Radiation Science as an Assistant Professor in 2013. Dr. Amiel is committed to working with undergraduate students both in the classroom and in the laboratory, and enjoys training students in scientific research. He is scheduled to teach the undergraduate Immunology course at UVM in the spring semester of 2014.
Postdoctoral training, Trudeau Institute, Saranac Lake, NY. (Lab or Dr. Edward Pearce 2009-2012, Lab of Dr. Elizabeth Leadbetter 2012-2013)
Ph.D., Geisel School of Medicine, Dartmouth College, Hanover, NH. (Lab of Dr. Brent Berwin 2004-2009)
BA, Biology and Philosophy, Amherst College, Amherst, MA. (Honors research thesis with Dr. David Ratner 2001-2002)
The study of inflammation, the specific activation of immune cells in response to pathogenic or toxic stimuli, is fundamentally important to understanding how the body neutralizes infections and combats chronic inflammatory stress. Research in the Amiel Laboratory focuses on studying the basic molecular mechanisms regulating cellular immune activation with the long-term goal of discovering new therapeutic approaches to manipulate immune responses to better meet the needs of immune-related clinical challenges. In the field of immunology, there is a growing appreciation of the importance of how metabolic changes in immune cells shape the types of immune responses that these cells perform. Of particular interest is the notion that manipulation of cellular metabolism can dramatically influence the type and magnitude of pathogen-specific immune responses.
The primary objective of our research proposal is to identify novel mechanisms of molecular control of cellular metabolism, and determine how these influence the activation and immune-generating potential of dendritic cells (DCs). DCs are immune cells that are important regulators of inflammation and also possess a vital function in initiating adaptive immune responses via their ability to acquire and present antigens to T lymphocytes. Prior to activation, DCs exist in a relatively quiescent metabolic state. Upon activation, DCs undergo a process of maturation that is accompanied by a profound metabolic switch in which they exhibit reduced mitochondrial function and up-regulate aerobic glycolysis. Our work focuses on elucidating some of the mechanisms responsible for inducing this metabolic switch and how these changes in DC metabolism influence the immune activation of these cells. The Amiel Laboratory uses a diverse investigative approach that includes cell biology, molecular, and biochemical approaches to investigate how metabolic signals control immune activation and function of dendritic cells.
Amiel E, Everts B, Freitas TC, King IL, Curtis JD, Pearce EL, Pearce EJ. Inhibition of mTOR Promotes Dendritic Cell Activation and Enhances Therapeutic Vaccination in Mice. J Immunology. 2012 Sep 1;189(5):2151-8.
Everts B, Amiel E, van der Wint GJW, Freitas TF, Chott R, Yarasheski KE, Pearce EL, Pearce EJ. Commitment to Glycolysis Sustains Survival of Nitric Oxide-producing Inflammatory Dendritic Cells. Blood. 2012 Aug 16;120(7):1422-31.
Huang SC, Freitas TF, Amiel E, Everts B, Lok JB, Pearce EL, Pearce EJ. Fatty Acid Oxidation is Essential for Egg Production by the Parasitic Flatworm Schistosoma mansoni. PLoS Pathogens. 2012;8(10):e1002996.
van der Windt GJW, Everts B, Chang C, Curtis JD, Freitas TC, Amiel E, Pearce EJ, Pearce EL. Mitochondrial Respiratory Capacity Is A Critical Regulator Of CD8 T Cell Memory Development. Immunity. 2012 Jan 27;36(1):68-78.
Krawczyk CM, Holowka T, Sun J, Blagih J, Amiel E, DeBerandinis RJ, Cross JR, Jung E, Thompson CB, Jones RG, Pearce EJ. Toll-like receptor induced changes in glycolytic metabolism regulate dendritic cell activation. Blood. 2010 Jun 10;115(23):4742-9.
Amiel E, Lovewell R, Berwin B. Non-motile Pseudomonas aeruginosa Bacteria are Resistant to Innate Immune Recognition and Phagocytosis. Infect. Immun. 2010 Jul;78(7):2937-45.
Amiel E, Acker J, Collins R, Berwin B. Uncoupling Scavenger Receptor-A –Mediated Phagocytosis of Bacteria from Endotoxic Shock Resistance. Infect. Immun. 2009 Oct;77(10):4567-73.
Amiel E, Alonso A, Uematsu S, Akira S, Poynter ME, Berwin B. Pivotal Advance: Toll-like receptor regulation of scavenger receptor–A–mediated phagocytosis. J Leukoc Biol. 2009 Apr;85(4):595-605.
Amiel E, Nicholson-Dykstra S, Walters JJ, Higgs H, Berwin B. Scavenger receptor-A functions in phagocytosis of E. coli by bone marrow dendritic cells. Exp. Cell Res., 2007 Apr 15;313(7):1438-48.