Department of Immunology, University of Toronto
Toronto,
ON
Canada
Biographical Sketch: Dr. Philpott completed her graduate work with a PhD in Medical Genetics and Microbiology at the University of Toronto, working on the mechanisms of pathogenesis of enteropathogenic Escherichia coli, under the supervision of Dr. Phil Sherman at the Hospital for Sick Children. She then pursued post-doctoral training at McMaster University with Dr. Mary Perdue followed by a fellowship at the Institut Pasteur in Paris, France, with Dr. Philippe Sansonetti. Here, she studied host cell responses to Shigella flexneri infection and began working on Nod-like receptors (NLRs). She became an independent group leader at the Institut Pasteur in 2002 and then accepted a position in the Department of Immunology at the University of Toronto in 2006. Dr. Philpott is currently an Associate Professor in the Department of Immunology where she focuses her work on understanding how bacteria are detected by the NLRs, Nod1 and Nod2, and how this initiates the immune response. Because of the link between Nod2 and Crohn’s disease, much of Dr. Philpott’s research is focused on understanding how dysregulation of Nod2 signaling impacts on mucosal homeostasis in the intestine.
Papers:
Nod-Like Receptors - At the Interface of Immunity and Microbes
OR.6
Intrinsic Regulation of Ileal Epithelial Cell Proliferation by the Bacterial Peptidoglycan Sensor Nod2
T.60
Microbiota Sensing by Nod2 Regulates Mucosal Damage in Small Intestinal Crypt Following Acute T cell Activation.
T.62
Conditional Epithelial Deletion of the Pathogen Recognition Receptor Nod2 Fails to Alter the Regulation of T cell-Induced Enteropathy
W.9
the Role of CD103+ Conventional Dendritic Cells in Host Antiviral Responses in the Gut
W.95
NOD2 Does Not Influence Bacterial Community Structure in the Salmonella ΔaroA Chronic Inflammation Model
W.118
Antibiotic Manipulation of the Adult Murine Microbiota Has Long-Term Effects on the Mucosal Immune Response in NOD2-/- Mice
W.120
Early Life Antibiotics Alters the Development of the Gut Microbiota and Mucosal Immune T cell Populations