＜シンポジウム03―3＞脱髄性疾患におけるグリア間およびグリア・ニューロン間相互作用の破綻
視神経脊髄炎，多発性硬化症，Baló病におけるアストロサイト障害の特徴
松下 拓也1）, 眞﨑 勝久2）, 鈴木 諭3）, 松岡 健2）3）, 米川 智2）, 呉 暁牧4）, 田平 武5）, 岩城 徹3）, 吉良 潤一2）
1）九州大学大学院医学研究院寄附講座臨床神経免疫学〔〒812―8582 福岡市東区馬出3―1―1〕
2）同 神経内科学
3）同 神経病理学
4）江西省人民医院神経内科
5）順天堂大学大学院認知症診断・予防・治療学
Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) while neuromyelitis optica (NMO) is an inflammatory disease of the CNS that selectively affects the optic nerves and spinal cord. An antibody for aquaporin-4 (AQP4), which is a water channel located in astrocyte foot process, is specifically positive for NMO and antibody and complement dependent astrocytic damage is thought to be a main cause of NMO. Baló's disease is characterized by alternating rings of demyelination and preserved myelin. We pathologically compared the astrocytic changes among autopsied cases with these CNS demyelinating diseases. NMO, MS and Baló's disease shared with reduced AQP4 immunoreactivity independent of antibodies and complements. The pathological finding was accompanied with a reduced immunoreactivity of connexin 43 and perivascular lymphocytic cuffing predominantly composed by T cells. The loss of astrocytic proteins such as AQP4 and connexin 43 preceded the loss of myelin proteins in some lesions. These features suggest astrocyte damages resulting in the loss of connexin 43 cause demyelination through the impairment of interaction between astrocytes and oligodendrocytes and the pathomechanism involves a T cell reaction.
Full Text of this Article in Japanese PDF (309K)
(臨床神経, 51：898－900, 2011)
key words：アストロサイト傷害，多発性硬化症，視神経脊髄炎，Baló病，コネキシン43
（受付日：2011年5月19日）
