본문 바로가기 주메뉴 바로가기 하위메뉴 바로가기

WORLD CLASS S&T UNIVERSITY

Academics

College of Life Science and Bioengineering

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.

Academic Degree Curriculum
Academic Degree Curriculum
Department/Major Bachelor's Courses Master's Courses Doctoral Courses Office of Academic Affairs Website
Department of Biological Sciences
042-350-2602(F.2610) Homepage go
Graduate School of Medical Science and Engineering
  042-350-4232(F.4240) Homepage go
Interdisciplinary Majors and Educational Programs
Education Program
College
(Department/Major)
Interdisciplinary Majors and Educational Programs Bachelor's Courses Master's Courses Doctoral Courses Office of Academic Affairs Website
Graduate School of Medical Science and Engineering
Biomedical Science and Engineering
Interdisciplinary Program
  042-350-4232(F.4240) Homepage go
※ Department of Bio and Brain Engineering is changed of affiliation from College of Life Science and Bioengineering to College of Engineering on March 1st, 2015.
KAIST COMPASS in Life Science & Bioengineering
2017 Fall Archeological traces of embryo development in adult  Architecture of a gatekeeper translocating Structural determinations shed light on MDGA Overturning conventional thinking in Parkinson’s ATP-dependent chromatin remodeler Ino80 replaces 2017 Spring A mechanism for the induction of type 2 immune responses by a protease allergen in the genital tract Auditory-to-visual feedforward inhibition mediates auditory dominance during the integration of audiovisual conflict Somatic Mutations in TSC1 and TSC2 cause focal cortical dysplasia. Reconstruction of LPS transfer cascade reveals structural determinants within LBP, CD14, and TLR4-MD2 for efficient LPS reconstruction and transfer How the retina fine-tunes brightness
News
 
Cellular Mechanism for Severe Viral Hepatitis Identified

Cellular Mechanism for Severe Viral Hepatitis Identified
(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.

 


Cellular Mechanism for Severe Viral Hepatitis Identified



(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.)

Cellular Mechanism for Severe Viral Hepatitis Identified
(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.)

Newsletter
Department of Biological Sciences KAIST COMPASS
Contact Information for the College of Life Science and Bioengineering: 042-350-ext.

Office of the Dean of the College of Life Science and Bioengineering: 2125
College of Life Science and Bioengineering Academic and Student Affairs Team: 1401, 1409, Fax: 1400

KAIST, 291 Daehak-ro, Yuseong-gu, Daejeon 34141, Republic of Korea

T. 042-350-2114 / F. 042-350-2210 (2220)

Copyright (C) 2014, Korea Advanced Institute of Science and Technology, All Rights Reserved.