Transcriptional Regulation of Proinflammatory Lymphocytes
IL-17-expressing CD4 T helper (Th17) cells are important members of the intestinal immune cell community that contribute to protection against bacterial and fungal infections, and maintenance of intestinal homeostasis. Although central to immunity, dysregulted Th17 cell function has been implicated in tissue inflammation and autoimmune disease (e.g. Inflammatory bowel disease, arthritis, and multiple sclerosis). In order to understand this balance between healthy and pathogenic responses, we are interested in defining the transcriptional regulatory mechanisms that govern (1) Th17 cell specification from naive T cell precursors and, (2) Th17 cell effector plasticity during inflammation. Combining genome-wide interrogation of regulatory information (transcription factor occupancy, chromatin accessibility, and transcriptional output) with gene-deficiency models in mice, we can dissect the contribution of key transcriptional regulators in proinflammatory T cell function.
We currently have open positions for students, postdoctoral fellows and a research technician.
Education and Training
- University of Toronto (Canada), Ph.D. 2007
Selected Grants and Awards
- Transplant Infectious Diseases Interdisciplinary Research Training Grant
- Regulatory Mechanisms of CD4+ T Cell Differentiation
- The role of AP-1 family transcription factor networks in regulating Th17 cell effector identity
- Molecular Mycology and Pathogenesis Training Program
- Basic Immunology Training Program
- Network approach to dissecting genetic mediators of Multiple Sclerosis