＜シンポジウム（3）―13―1＞脱髄性疾患の病態に基づいた新規治療戦略
オリゴデンドロサイトパチーと新たな髄鞘再生戦略
中原 仁
慶應義塾大学医学部神経内科〔〒160―8582 東京都新宿区信濃町35〕
Spontaneous remyelination occurs in many early multiple sclerosis (MS) patients, however its capacity decreases as the disease becomes chronic. Even in those chronic MS patients, an enough number of oligodendrocyte precursor cells (OPCs) are preserved within the demyelinated lesions, suggesting that the differentiation arrest of oligodendroglial cells underlies the remyelination failure in chronic MS. We have previously reported that TIP30, a factor inhibiting nucleocytoplasmic transport within the cell, is responsible for the differentiation arrest in MS lesions. Overexpression of TIP30 in the preserved OPCs in MS lesions results in the failure of nuclear translocation of transcription factors necessary for oligodendroglial differentiation. Therefore, anti-TIP30 therapy to regain the nuclear access within the OPCs is necessary for sufficient remyelination in chronic MS patients. Moreover, inflammatory conditions surrounding OPCs may be involved in the efficient remyelination in early MS lesions, alternative stimulatory factor may therefore be mandatory to induce OPC differentiation into oligodendrocytes within the chronic lesion. We have previously reported that targeting FcRγ protein on OPCs may stimulate their differentiation and consequently remyelination in the chronic lesions. A timely collaboration of these two approaches may be required for successful remyelination and neurological recovery in chronic MS patients.
Full Text of this Article in Japanese PDF (239K)
(臨床神経, 52：1351−1353, 2012)
key words：多発性硬化症，オリゴデンドロサイトパチー，髄鞘再生，TIP30，FcRγ
（受付日：2012年5月25日）
