Biographical Sketch

Dr. Kim received his BS degree in zoology from Seoul National University in 1967, MS degree in microbiology from Virginia State University in 1969, and PhD degree in microbiology and immunology from the University of Illinois in 1973. His PhD work was on the regulation of antibody production. He continued his postdoctoral training in retrovirology with Dr. Sol Spiegelman at Columbia University, and then took further training in immunoregulation with Dr. Donald Rowley at University of Chicago.

Research Description

The mechanisms involved in immune-mediated demyelination following infection with Theiler’s virus are investigated in our laboratory as a model system for human multiple sclerosis.  Specific lines of investigations include: mechanisms of cellular gene activation by virus infection and consequent effects on viral replication and immune response development; role of helper T cell types and specificity and repertoires involved in the protection or pathogenesis of demyelinating disease; role of cytotoxic T cells in the CNS and periphery in protection and/or pathogenesis of demyelination in susceptible and resistant mice.   

Research Abstract

Our laboratory is engaged in studies on the pathogenic mechanisms involved in virus-induced demyelinating disease. We focus on three different areas of the pathogenic mechanisms. First, the mechanisms involved in the initial induction of inflammatory responses upon virus infection, including cytokine and chemokine genes directly activated in glial cells. We have identified for the first time several cytokines and select chemokine genes activated in primary astrocyte cultures upon Theiler’s virus infection. The signal transduction mechanisms of cellular gene activation by viral infection are also being actively investigated. We have found that activation of these cellular genes is dependent on NFkB and are currently determining the upstream signals as well as influence of NFkB deficiency on disease susceptibility. In addition, we are investigating the potential role of virus-activated glial cells for the initiation of virus-specific adaptive immune responses, as well as spreading viral infection and promoting viral replication. Second, we investigate viral determinants recognized by the adaptive immune system including cytotoxic and helper T cells and their role in the protection and/or pathogenesis of demyelinating disease. We have identified several such viral determinants recognized by T cell subpopulations in susceptible as well as resistant mouse strains. In addition, several recombinant viruses modified in immune recognition sites and transgenic mice expressing viral antigens have been generated.  In addition, transgenic mice expressing T cell receptors specific for viral determinants have also been recently generated. These mice are being utilized to study the role of these viral and T cell compartments as well as the sites for T cell expansion and repertoire selection in protection and/or pathogenesis of demyelination. Third, we examine the role of gender and sex hormones in the pathogenesis of virally induced demyelinating disease. In this viral model, males are more susceptible than female mice, opposite to the observed gender bias in human MS. We are dissecting the underlying mechanisms of the differences between human disease and this virus model. We are currently investigating the mechanisms and immune compartments affected by sex hormones.

Publications

Kwon, D., Fuller, A. C., Palma, J. P., Choi, I.-H., and Kim, B. S.: Induction of chemokines in human astrocytes by picornavirus infection requires activation of both AP-1 and NFkB.  Glia 45:287-296, 2004.

Palma, J. P. and Kim, B. S.: The scope and activation mechanisms of chemokine gene expression following infection with Theiler’s murine encephalomyelitis virus.  J. Neuroimmunol. 149: 121-129, 2004.

Lyman, M. L., Myoung, J., Mohindru, M., and Kim, B. S.: Quantitative, not qualitative, differences in CD8⁺ T cell responses to Theiler's murine encephalomyelitis virus between resistant C57BL/6 and susceptible SJL/J mice.  Eur. J. Immunol. 34: 2730-2739, 2004.

Kim, B. S., Palma,J. P., Kwon, D., and Fuller, A. C.: Innate immune response induced by Theiler’s murine encephalomyelitis virus infection. Immunol. Res. 3:1-12, 2005.

Kang, B., Kang, H.-K., and Kim, B. S.: Identification of capsid epitopes of Theiler’s virus recognized by CNS-infiltrating CD4⁺ T cells from virus-infected C57BL/6 mice. Virus Research, 108:57-61, 2005.

Kang, B., Palma, J. P., Lyman, M. L., Lee, H.-G., DalCanto, M., and Kim, B. S.: Antibody response is not essential for protection from Theiler’s virus-induced demyelination in C57BL/6 mice. Virology 340:84-94, 2005.

Kim, B. S., Mohindru, M., Kang, B., Kang, H. and Palma, J. P.: Effects of the major hostocompatibility complex loci on T cell repertoire and Theiler’s virus-induced demyelinating disease. J. Neurosci. Res. 81:846-856, 2005.