Jun Yong Lee
Yonsei University
About the Lab
Professor Jun Yong Lee's research lab focuses on immunometabolism, particularly the interplay between metabolic reprogramming and immune responses in health and disease. The lab investigates novel food allergens, such as those from silkworm pupa, using proteomic and molecular approaches to understand allergic sensitization mechanisms. Another key direction involves the role of intestinal lipid-binding proteins, like ileal lipid-binding protein (Ilbp), in maintaining bile acid homeostasis and regulating gut inflammation through microbiota interactions. The lab integrates systems biology, metabolomics, and immunology to explore how metabolic pathways modulate immune function and contribute to inflammatory diseases.
Research Overview
Research Output Trend
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Selected Papers
3Boiled silkworm pupa is a traditional food in Asia, and patients with silkworm pupa food allergy are common in these regions. Still now only one allergen from silkworm, arginine kinase, has been identified. The purpose of this study was to identify novel food allergens in silkworm pupa by analyzing a protein extract after heat treatment. Heat treated extracts were examined by proteomic analysis. A 27-kDa glycoprotein was identified, expressed in Escherichia coli, and purified. IgE reactivity of
Metabolic regulation is one of the key factors in the direct or indirect control of immune responses. The term “immunometabolism” refers to the study of how metabolic pathways regulate immune responses. This field has gained significant attention over the past few decades, particularly with advances in systems biology, metabolomics, and immunology (1). In addition to the direct regulation of immune cells by metabolic pathways, immune cell- or immune factor-mediated metabolic regulation during in
Ileal lipid binding protein (Ilbp), encoded by Fabp6 gene, plays a critical role in intracellular transport of bile acids (BAs) from apical to basolateral side of ileal enterocytes, maintaining BA homeostasis within enterohepatic circulation. However, pathophysiological consequences of Ilbp deficiency remain largely unexplored. Here, we demonstrate that disruption of BA balance, caused by intestinal epithelial cell (IEC)-specific Fabp6 gene knockout (Fabp6ΔIEC), exacerbates dextran sulfate sodiu
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