With the specialization of biology, brain science, medical science, and IT/NT, KAIST has accumulated academic capability in the area of biology. The College of Life Science and Bioengineering was founded to efficiently support the fusion research environment of KI for Biocentury at KAIST.
The College of Life Science and Bioengineering is composed of the Department of Biological Sciences, Department of Bio & Brain Engineering, and Graduate School of Medical Science & Engineering. The college pursues multidisciplinary education & research in the area of biology and the development of modern science through the fusion of the IT & NT foundation techniques for the development of the nation’s biological science and technology.
The Department of Biological Sciences fosters scientists and engineers of life science and biotechnology equipped with creative research skills to lead in the development of science and technology in the area of biological sciences and excellent scientists equipped with future oriented thinking and a holistic personality.
The multidisciplinary Department of Bio & Brain Engineering fosters a creative workforce that is capable of creating new knowledge and techniques in the fusion areas of electronics, computers, and nanotechnology based on biomedical science.
The Graduate School of Medical Science & Engineering is catered to doctors (specialists), graduates from medical schools, dental schools, and schools of oriental medicine for the development of new medicine and medical devices. The Graduate School of Medical Science & Engineering was established with the purpose of developing life sciences and medical technology and fostering a high-quality workforce equipped with a multidisciplinary knowledge in basic medicine, life science, and biomedical engineering, as well as research experience.
(Professor Shin(left) and Professor Jung)
KAIST medical scientists identified a cellular mechanism causing inflammatory changes in regulatory T cells that can lead to severe viral hepatitis. Research on this mechanism will help further understand the nature of various inflammatory diseases and lead to the development of relevant clinical treatments.
It is known that activated immune cells of patients with viral hepatitis destroy hepatocyte, but its regulatory mechanism has not yet been described.
Regulatory T cells inhibit activation of other immune cells and thus are important for homeostasis of the immune system. However, recent studies contradictorily show that immune inhibitory functions of regulatory T cells weaken in inflammatory conditions and the cells secrete inflammatory cytokines in response. Meanwhile, such a phenomenon was not observed in viral hepatitis including types A, B and C.
The team focused on changes in regulatory T cells in patients with viral hepatitis and discovered that regulatory T cells undergo inflammatory changes to secrete inflammatory cytokines (protein secreted by immune cells) called TNF. They also proved regulatory T cells that secrete TNF contribute to the progression of viral hepatitis.
The team confirmed that regulatory T cells of acute hepatitis A patients have reduced immune-inhibitory functions. Instead, their regulatory T cells secrete TNF. Through this research, the team identified a molecular mechanism for changes in regulatory T cells and identified the transcription factor regulating the process. Furthermore, the team found similar changes to be also present in hepatitis B and C patients.
A KAIST immunology research team led by Professors Eui-Cheol Shin and Min Kyung Jung at the Graduate School of Medical Science & Engineering conducted this translational research with teams from Chungnam National University and Yonsei University to identify the mechanism in humans, instead of using animal models. The research was described in Gastroenterology last December.
Professor Shin said, “This is the first research on regulatory T cells that contributes to hepatocyte damage in viral hepatitis.” He continued, “It is significant for identifying the cells and the molecules that can be used as effective treatment targets for viral hepatitis in the future. This research was funded by the Samsung Science and Technology Foundation.
(Figure1: Treg cells from acute hepatitis A (AHA) patients produce tumor necrosis factor (TNF) andhave reduced suppressive activity. These changes are due to a decrease in FoxP3 transcription factor and an increase in RORγt transcription factor. TNF-producing Treg cells are associated with severe liver injury in AHA patients.)
(Figure 2: A higher proportion of Treg cells from patients with acute hepatitis A, compared with healthy controls, produced TNF upon stimulation with anti-CD3 and anti-CD2. This study reports the presence and the significance of TNF-producing Treg cells for the first time in human patients.)
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