Ulsan National Institute of Science and Technology · 医学
Professor Sung Ho Park's research lab focuses on the immunological mechanisms underlying chronic inflammatory diseases, with a central emphasis on macrophage and T cell biology in conditions such as atherosclerosis, allergic asthma, and severe viral infections like COVID-19. The lab investigates how metabolic and redox signals—particularly reactive oxygen species (ROS) and the NRF2 pathway—regulate immune cell function and phenotype plasticity, especially in the context of tissue inflammation and immune cell heterogeneity. A key research direction involves understanding how innate immune responses transition from protective to pathological, contributing to disease progression and severity. The lab integrates preclinical models with human immunology to identify novel therapeutic targets for inflammatory and immune-mediated diseases.
Figures are computed from collected data and may differ slightly.
Chronic inflammation is a hallmark of atherosclerosis and macrophages play a central role in controlling inflammation at all stages of atherosclerosis. In atherosclerosis, macrophages and monocyte-derived macrophages are continuously exposed to cholesterol, oxidized lipids, cell debris, cytokines, and chemokines. Not only do these stimuli induce a specific macrophage phenotype, but they also interact extensively, leading to macrophage heterogeneity in atherosclerotic plaques. Herein, we review t
The recent appearance of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has affected millions of people around the world and caused a global pandemic of coronavirus disease 2019 (COVID-19). It has been suggested that uncontrolled, exaggerated inflammation contributes to the adverse outcomes of COVID-19. In this review, we summarize our current understanding of the innate immune response elicited by SARS-CoV-2 infection and the hyperinflammation that contributes to disease severity
Upon encountering allergens, CD4<sup>+</sup> T cells differentiate into IL-4-producing Th2 cells in lymph nodes, which later transform into polyfunctional Th2 cells producing IL-5 and IL-13 in inflamed tissues. However, the precise mechanism underlying their polyfunctionality remains elusive. In this study, we elucidate the pivotal role of NRF2 in polyfunctional Th2 cells in murine models of allergic asthma and in human Th2 cells. We found that an increase in reactive oxygen species (ROS) in imm
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