Characterization of Intestinal Dendritic cells
The intestine maintains immune homeostasis despite continuous exposure to microbial and dietary antigens. Lamina propria dendritic cells (LP-DCs) play a pivotal role in balancing Treg and Th17 cells, with Th17 induction enhancing intestinal barrier function. However, how LP-DCs acquire this ability, along with their distinct characteristics, remains poorly understood. Our research focuses on identifying the key factors and mechanisms regulating LP-DC functions, with the goal of uncovering the drivers of intestinal inflammation and potential therapeutic targets.
GPR43-mediated immune-regulation
Dietary fiber is indigestible in humans due to a lack of necessary enzymes, so it reaches the cecum and colon. Gut microbes ferment fiber, producing short-chain fatty acids (SCFAs). One of the receptors for SCFAs, GPR43, is highly expressed in immune cells. SCFAs can interact with GPR43 in immune cells and potentially influence the immune system. However, the exact effects and mechanisms of this interaction remain unclear. Our lab aims to elucidate the role of GPR43 in immune cells such as eosinophils and neutrophils using various disease models and genetically modified mice, and to uncover the underlying mechanisms.
TFEB-mediated immune-regulation
Transcription factor EB (TFEB), a member of the MiT/TFE family of basic helix-loop-helix leucine-zipper transcription factors, is best known as a master regulator of autophagy and lysosome-associated genes. It dynamically shuttles between the lysosomal surface, the cytosol, and the nucleus. Cellular stressors, such as starvation, ER stress, lysosomal and mitochondrial dysfunction, and reactive oxygen species (ROS), trigger TFEB's nuclear localization and activation. Recently, TFEB has been recognized for its broader roles in regulating glucose and lipid metabolism, as well as immune responses. Our lab focuses on elucidating the role of TFEB across different immune cell types, aiming to uncover novel regulatory mechanisms that impact both metabolism and immunity.
Effect of Latent viral infection on Metabolic diseases
Metabolic-associated fatty liver disease (MAFLD) affects 30-40% of the global population, with prevalence on the rise. This growing burden emphasizes the need to explore its relationship with other conditions. Cytomegalovirus (CMV), with infection rates ranging from 60-99% worldwide, is often asymptomatic in healthy individuals but induces significant immunological changes, such as memory T cell inflation and senescence. Our lab has discovered these CMV-driven immune alterations can accelerate the progression of MAFLD. We are actively investigating the underlying immunological mechanisms that link CMV infection to the advancement of MAFLD, aiming to uncover key insights that could lead to new therapeutic strategies.
Commensal bacteria-based Cancer immunotherapy
The gut microbiome, a diverse community of microorganisms including bacteria, archaea, viruses, and eukaryotic microbes, plays a key role in shaping host immunity. The distinct microbial composition and their higher mutation rates contribute to inter-individual variability, resulting in differential success of immune checkpoint blockade (ICB) therapy. Especially, bacteria-derived extracellular vesicles (bEVs), which mimic the properties of their parent bacteria without proliferative capacity, have garnered attention for their potential in cancer treatment. Our lab investigates how these bEVs activate immune cells to suppress tumor progression, aiming to uncover the molecular mechanisms that drive their anti-tumor effects within the tumor microenvironment.
Greaduate School of Medical Science & Engineering
Korea Advanced Institute of Science and Technology
291 Daehak-ro, Yuseong-gu
Daejeon 34141 Republic of Korea