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Ae-Kyung Yi, PhD

Ae-Kyung Yi, PhD
Professor
858 Madison Ave.
Room 501C
Memphis, TN 38163
ayi@uthsc.edu
Phone: 901.448.1775
Fax: 901.448.7360

Education

  • PhD, University of Wisconsin-Milwaukee, 1993
  • MS, Hanyang University, 1987
  • BS, Hanyang University, 1985

Research Interests

The immune system has evolved to efficiently protect the body from many forms of foreign invasions.  The immune response has been shown to play a key role in modulating the pathogenesis of many diseases.  Understanding how the immune system responds to the microbial products and the altered-self products might contribute to finding ways to control the diseases more effectively.  I am interested in the signaling events involved in activation and deactivation of immune cells by pathogen-associated molecular patterns (PAMPs: microbial products) and danger-associated molecular patterns (DAMPs: altered-self products), and contributions of the pattern recognition receptor (PRR)-mediated signaling in the host defense and inflammatory autoimmune diseases. The long-term goals of my research are to understand Toll-like receptor (TLR; one of PRRs) signaling pathways in different types of immune cells, and the specific function of each signaling modulator in TLR signaling pathways in the orchestration of innate immune activation and deactivation process during the course of inflammation and inflammatory autoimmune disease.  Currently, research in my laboratory is focused on two projects.  First, we are investigating molecular mechanisms of protein kinase D1 [PKD1; a serine/threonine kinase activated by most TLRs and interleukin 1 receptor (IL-1R)] activation and action in the TLR/IL-1R signaling pathway, role of PKD1 in the pathogenesis of inflammatory diseases using animal models of inflammatory autoimmune arthritis and hypersensitivity pneumonitis, and whether PKD1 can be an effective therapeutic target for inflammatory autoimmune arthritis. We are also developing a peptide-based PKD1 inhibitor and a nanosome-based inflammation site-specific drug delivery system with our collaborators on campus. Second, we are investigating action mechanisms of a natural inhibitor receptor called leukocyte associated immunoglobulin-like receptor-1 (LAIR-1; CD305) for attenuating T cell receptor signaling and TLR/IL-1R signaling, role of LAIR-1 in the pathogenesis of inflammatory autoimmune arthritis, and whether and how expression of LAIR-1 can be modulated in immune cells by anti-inflammatory agents.   

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Last Published: Mar 12, 2021