第49回日本神経学会総会
＜シンポジウム4-4＞多発性硬化症の病態と治療：臨床と基礎の最前線
治療法の開発をめざして「基礎からの展望」
錫村 明生
名古屋大学環境医学研究所神経免疫分野〔〒464-8601 名古屋市千種区不老町〕
The pathogenesis of multiple sclerosis (MS) remains to be elucidated and there is no curative therapy against MS, though we have several disease modifying drugs. In this symposium, I introduce several new strategies against development of autoimmune processes and axonal degeneration in MS. Several mechanisms regulate immune system not to attack self components. One of the most potent regulatory cells is CD4 + CD25 + FoxP + regulatory T cells (Treg), which suppress development of both T helper 1 and 2. Thus, to increase the number and function of Treg is an approach to suppress autoimmune diseases. We have found recently that midkine suppresses the development of Treg, and that suppression of midkine by RNA aptamer alleviates symptoms of experimental autoimmune encephalomyetitis, an animal model of MS, by expanding Treg. Another important strategy against MS is to suppress axonal degeneration which reportedly occurs from an early stage of MS. We have found that the most toxic agent from activated macrophages and microglia is glutamate that was produced by glutaminase and released through gap-junction. Thus, inhibitor for glutaminase and gap-junction may be other candidates to treat MS. Interferon-β also effectively suppress glutamate production by these cells and subsequently suppress development of axonal degeneration.
Full Text of this Article in Japanese PDF (265K)
(臨床神経, 48：937−939, 2008)
key words：多発性硬化症, 自己免疫, 制御性T細胞, 軸索変性, ミクログリア
（受付日：2008年5月16日）
