@techreport{oai:kindai.repo.nii.ac.jp:02000403,
 author = {佐藤, 文孝 and Sato, Fumitaka},
 note = {本研究では，ヒト多発性硬化症(MS)の中枢神経系(CNS)病理像と同様にヘルパーT(Th)17細胞とCD8+T細胞の浸潤を伴うタイラーウイルス誘導性脳脊髄炎(TMEV-IDD)を用い，MS病態の解明を行った。Th17細胞を増強するとTMEV-IDDが軽減し，かつCD8+T細胞関連の遺伝子発現がCNS内で減少した。またこの一連の研究を通して，IgA抗体がCNS内に沈着しているのを見出した。近年、IgA産生B細胞の浸潤がMSでも報告されており，本成果からMS病態におけるTh17細胞－CD8+T細胞－IgA抗体による新規のコミュニケーションが明らかとなり，新たな治療法の開発へつながる可能性を示した。, Multiple sclerosis (MS) is an immune-mediated disease in the central nervous system (CNS). Although helper T (Th) 17 cells have been suggested to play pathogenic roles in MS, the precise pathomechanisms are unclear. We have used a viral model of MS, Theiler’s murine encephalomyelitis virus (TMEV) infection in mice, in which we can see infiltration of Th17 and CD8+T cells in the CNS that resembles MS neuropathologically. In this study, using the viral model, we aimed to determine the pathogenesis of MS by treating mice with a Th17 modulator, curdlan. Compared with control mice, curdlan-treated mice had significantly less severe clinical signs with decreased levels of CD8+ T cells and granzyme B in the CNS. We also found lower levels of IgA deposition in the CNS demyelinating lesions in curdlan-treated mice. Since IgA-producing B cells have been detected in the CNS of MS patients, our findings suggest the novel interactions among Th17, CD8+ T-cell, and IgA responses in MS., 研究分野：神経免疫学},
 title = {MS疾患モデルでのTh17／CD8+ T細胞間の新規コミュニケーションと併用療法}
}