[S-02] Genetic and neuropathological approach decipher the molecular mechanism of idiopathic central nervous system demyelinating diseases

[S-02-4] Disease-specific TCRs recognize CMV in Japanese MS with HLA-DRB1*04:05; a novel approach with GLIPH

林 史恵¹, 磯部 紀子², Jacob Glanville³, 中村 優理², 松下 拓也¹, 吉良 潤一¹ (1.九州大学医学研究院脳神経内科学, 2.九州大学医学研究院脳神経治療学, 3.Computational and Systems Immunology Program, Stanford University School of Medicine)

Genome-wide association studies (GWAS) on multiple sclerosis (MS) in Caucasians have identified various risk genes, which are mainly related to immune functions. Molecular pathways leading to inflammatory demyelination are now becoming clearer. The first Japanese GWAS, enrolling more than 1,000 MS and neuromyelitis optica spectrum disorders (NMOSD) patients, has revealed the distinct risk genes from those in Caucasians, many of which are related to neuroglial functions. Molecular-immunopathological studies have also identified critical changes of glial cells in these conditions. Therefore, the aim of this symposium is to decipher the mechanisms of the MS and NMOSD by integrating the functions of the discovered genetic risk factors and the pathologically-proven molecular changes, with special attention on the demyelinating disorders more frequently encountered in Asians, such as NMOSD and Baló’s concentric sclerosis.

Education
-2010 M.D., Hokkaido University School of Medicine, Hokkaido.
2016-Present Ph.D., Department of Neurology, Graduate School of Medical Sciences, Kyushu University, Fukuoka.

Positions and Employment
2010-2012 Junior Resident in Iizuka Hospital, Fukuoka.
2012-2013 Senior Resident in General Internal Medicine, Iizuka Hospital, Fukuoka.
2013-2016 Fellow in Neurology, Kyushu University, Fukuoka.