Cellular and Molecular Mechanisms of Immune Tolerance in Health and Diseas
- Cellular and Molecular Mechanisms of Immune Tolerance in Health and Diseas
- IM, SIN HYEOG
- Date Issued
- Dr. Sin-Hyeog Im is a Professor in the Integrative Biosciences and Biotechnology & Department of Life Sciences, Pohang University of Science and Technology (POSTECH). He received his bachelor’s degree and master’s degree (Biochemistry) at Korea University, and Ph.D. degree (Immunology) at the Weizmann Institute of Science, Israel. During his PhD studies, he investigated to develop antigen specific immune tolerance to suppress the autoimmune responses. During his post-doc training under the guidance of Dr. Anjana Rao in the Harvard Medical School, he investigated molecular mechanism of T cell anergy. He joined GIST as an assistant professor in 2004, and has investigated molecular and cellular mechanism of immune tolerance in diverse immune cells. At the cellular level, he identified immunoregulatory bacteria that can induce high levels of IL-10 and immunoregulatory T cells (Treg) to suppress inflammatory immune responses. A probiotic consortium composed of 5 different strains (IRT5) could induce Treg cells in dendritic cell (DC) dependent manner, then migrate to the site of inflammation, and addressed the importance of gut microbiota in immune disorders [PNAS (2010). This paper has been highly cited (448 times) and considered as cutting-edge paper in probiotic research. To
further extend his findings at the molecular levels, he moved to POSTECH in 2014. Using the germ-free mouse facility, he further proved that Bifidobacterium bifidum PRI1 could induce Treg cells in the colon, and defined the molecular identity of Treg inducing activity. He proved that cell surface derived beta-glucan/galactan containing polysaccharides (CSGG) could induce diverse antigen-specific Treg cells, and paved a way to develop bacteria as a potential immunemodulatory drug (microbiome therapeutics) (Science Immunology, 2018). Moreover, he has investigated how a single faulty gene, Ets1, can lead to Lupus development. He reported that Ets1 is involved in controlling the expansion of a newly-described class of immune cells, known as T follicular helper type 2 (Tfh2) cells that produce pathogenic autoantibodies in mice and human SLE cases. Moreover, he also suggested that blocking of autoantibody production pathway could mitigate some SLE features emphasizing the need for alternative strategies targeting Tfh2 cells for lupus treatment (Immunity. 2018). Collectively, Dr. Im’s research will provide a close link between basic science and translational approach to treat hyper-immune responses such as autoimmune and allergic disorders.
- Article Type
- 한국분자세포생물학회 2019, 2019-10-02
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