Researcher | Research Overview
As the sensory system and immune system both serve a defensive function, and pain is a cardinal sign of inflammation, I wondered, how exactly do the nociceptive and immune systems interact, what factors might mediate communication between nociceptors and immune cells, and what in this communication goes awry in the pathology of pain syndromes. My postdoctoral project aims to clarify the interaction between the sensory system and the immune system and the consequences of this interaction for pain and immunopathology.
Researcher | Research Background
I received my B.A. in Molecular and Cell Biology from UC Berkeley in 2000, where I worked in Dan Portnoy’s lab studying virulence mechanisms of Listeria monocytogenes. After a year as a lab manager in the Baker Lab at the USDA, I entered the M.D., Ph.D. program at Yale and joined the lab of Dr. Ruslan Medzhitov in Immunobiology, where I explored the role of chromatin modifications in regulating different classes of inflammatory genes, and described a form of adaptability in the innate immune system. During my Ph.D. training, I gathered expertise in molecular biology and immunology, and was broadly exposed to fields ranging from microbial pathogenesis to autoimmunity to cancer surveillance.
After the Ph.D., I completed one year of internship in medicine at Mass General Hospital, then finished my clinical training in psychiatry at the University of Pennsylvania. As my clinical training progressed, I began to appreciate the huge clinical problem of chronic pain syndromes, which often come with heavy burdens of anxiety, depression, and sleep disturbance. Over my final year in residency, while working in a pain clinic, it became clear to me that our current treatments for pain are often ineffective or come with unacceptable side effects, and this inadequacy of treatment reflects our poor understanding of pain biology.