Korea Advanced Institute of Science and Technology · 医学
Professor Won-Il Jeong's research lab focuses on the immunological and cellular mechanisms underlying liver fibrosis, with a particular emphasis on the roles of innate immune receptors (such as TLR3), signaling molecules (like STAT1 and SOCS1), and immune cell crosstalk (including HSCs, γδ T cells, NK cells, and Kupffer cells) in disease progression. The lab investigates how endogenous ligands, exosomes, and metabolites (e.g., mtdsRNA) activate pathogenic inflammatory pathways in the context of alcoholic liver disease and cholestatic or toxic liver injury. A central theme is identifying novel therapeutic targets—such as TLR3, IFN-γ/STAT1 axis, and regulatory circuits involving IL-10—for fibrosis modulation.
Figures are computed from collected data and may differ slightly.
Liver fibrosis, a common scarring response to chronic liver injury, is a precursor to cirrhosis and liver cancer. Here, we identified signal transducer and activator of transcription 1 (STAT1) as an important negative regulator in liver fibrosis. Our findings show that disruption of the STAT1 gene accelerated liver fibrosis and hepatic stellate cell (HSC) proliferation in an in vivo model of carbon tetrachloride (CCl4)-induced liver fibrosis. In vitro treatment with IFN-gamma inhibited prolifera
In liver injury, the exosome-mediated activation of TLR3 in HSCs exacerbates liver fibrosis by enhancing IL-17A production by γδ T cells, which might be associated with HSC stimulation by unknown self-TLR3 ligands from damaged hepatocytes. Therefore, TLR3 might be a novel therapeutic target for liver fibrosis. (Hepatology 2016;64:616-631).
The antifibrogenic effects of NK cell/IFN-γ are suppressed during advanced liver injury, which is likely due to increased production of TGF-β and expression of SOCS1 in intermediately activated HSCs.
EtOH-mediated generation of mtdsRNA contributes to TLR3 activation in Kupffer cells through exosomal delivery. Consequently, increased IL-1β expression in Kupffer cells triggers IL-17A production in γδ T cells at the early stage that may accelerate IL-17A expression in CD4<sup>+</sup> T cells in the later stage of ALD. Therefore, mtdsRNA and TLR3 may function as therapeutic targets in ALD.
To date, the majority of research on hypercholesterolemia has focused on the effects of a high cholesterol diet on atherosclerosis and coronary heart disease. The toxic effects of cholesterol on the liver and the relationship between the intake of a high cholesterol diet and hepatic fibrosis, however, have not been investigated clearly or histopathologically. Male Wistar rats were fed a diet supplemented with 1.0% cholesterol and 0.3% sodium cholate for 12 weeks. Rats were sacrificed and analyze
Activated HSCs increase IL-10 expression in BMCs (CD11b(+) Gr1(high) F4/80(-) and CD11b(+) Gr1(+) F4/80(+) cells), which in turn ameliorates liver fibrosis. Our findings could enhance the design of BMC therapy for liver fibrosis.
The hepatic innate immune system consists of predominant innate immunity, which plays an important role in innate defense against infection and tumor transformation. Emerging evidence suggests that innate immunity also contributes to liver injury, repair, and fibrosis. The present review summarizes the recent findings on the role of innate immunity in liver fibrosis. In general, Kupffer cells stimulate liver fibrosis via production of reactive oxygen species and pro-inflammatory cytokines, where
mGluR5 plays important roles in attenuating liver fibrosis by augmenting NK cell cytotoxicity, which could be used as a potential therapeutic target for liver fibrosis.
Activated hepatic stellate cells (HSCs) have been considered as a major type of cells in liver fibrosis by producing a huge amount of extracellular matrix, especially collagen fibers, and profibrotic mediators such as transforming growth factor-beta, interleukin-6 and monocyte chemoattractant protein-1. Recently, accumulated evidence suggests that the liver is an immunologic organ because of enrichment of diverse types of immune cells and that their interactions with HSCs are closely related wit
Three dead dogs were brought to the College of Veterinary Medicine, Kyungpook National University for study. Clinically, all the dogs showed emaciation, anorexia, depression, hemorrhagic vomiting and diarrhea for 7-10 days before death. All the clinical signs were first noted for about one month after feeding the dogs with commercial diets. At necropsy, all 3 dogs had severe renal damage with the same green-yellowish colored nephroliths in the renal pelvis. They also showed systemic hemorrhage a
The numbers of macrophages and myofibroblasts increased in the development of fibrosis but decreased when cirrhosis was induced. However, mast cells increased in both. Therefore, there was a numerical relationship among the numbers of macrophages, myofibroblasts and mast cells in liver fibrosis but none between the former two cells and the mast cells in liver cirrhosis.
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