Postdoc: The Scripps Research Institute, San Diego, CA, USA
PhD: University of British Columbia, Canada
Office: Siebens Drake Research Institute, Room 119
Lab Website: http://www.kimlab-uwo.com/
Area of Study:
Our research program focuses on the signaling and epigenetic mechanisms of innate immune cells in responding to various microbes, tissue injury and cancers.
-Epigenetic regulation of inflammatory gene transcription
-Bacterial factors and macrophage immune regulation.
-Tumors and tumor-associated macrophages
Macrophages are sentinel innate immune cells residing in all tissues. They rapidly engulf and destroy foreign objects and microorganisms through phagocytosis. They also play a crucial role in sensing microenvironments to orchestrate immune responses through releasing various cytokines and chemokines. Because of tissue heterogeneity and ever-changing microenvironments, it is imperative for macrophages to be resilient to adapt and maintain immunological homeostasis. For example, primed (or trained) macrophages trigger rapid inflammatory responses against invading microbes, and harnessed (or tolerated) macrophages maintain quiescence with various commensal microbes. Unlike cells in homeostasis, overtly activated macrophages lead to inflammatory/autoimmune diseases; whereas, suppressed macrophages allow tumors to grow. Therefore, it is important to understand mechanisms by which macrophages senses and educate themselves to properly respond to unique environments. A key mechanism that attribute to their plastic characteristics is epigenetics that programs and re-programs gene transcription profiles. Our overall goal of research is to understand the signaling and epigenetic mechanisms of macrophages in sensing and educating during homeostatic and pathogenic conditions. Currently, our research focuses on two topics: 1. Signaling cascades that regulate histone acetylation-mediated epigenetic mechanisms involved in the tolerance of macrophages in response to bacterial components such as lipopolysaccharides and anthrax lethal toxin; 2. Role of transcription factors involved in epigenetic mechanisms of macrophage immune tolerance in tumor-associated microenvironment.