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  会員専用

• ホーム
• 50巻11号
• 臨床神経, 50：882−885, 2010
• 50巻11号目次

第51回日本神経学会総会

＜シンポジウム06―4＞脳血管障害治療の次のブレークスルーを目指して
脳梗塞後の炎症制御と神経再生

石橋　哲

東京医科歯科大学脳神経病態学〔〒113―8510 文京区湯島1―5―45〕

Neuroblasts in the subventricular zone proliferate markedly after stroke, and migrate to the site of injury along with blood vessels. However, a large fraction of stroke-generated neuroblasts die shortly after being born, because of local inflammation. E-selectin is specifically expressed on endothelial cells, but only when the endothelium activates. Since endothelial activation occurs after stroke, E-selectin can serve as an immunologic tolerization antigen that can focus immunomodulation to regions of the vascular tree. Intranasal instillation of recombinant E-selectin will induce mucosal tolerance to that antigen with the generation of E-selectin-specific regulatory T cells (Tregs). Tregs may protect newly-generated neuroblasts from ischemic damage through 'bystander suppression' in which immunomodulatory cytokines such as TGF-β and IL-10 are released locally. In this series of experiments, we have shown that after E-selectin tolerization in permanent middle cerebral artery occlusion (pMCAO) rats Tregs transmigrate to the peri-infarct region of ischemic brain, TNF expression in the local neurovascular niche is reduced, and the survival of newly generated neuroblasts or neurons in the peri-infarct region is increased. Under these conditions, an improvement in sensorimotor function after pMCAO also occurs. E-selectin-specific Tregs can modulate the efficacy of adult neurogenesis after ischemia and promote repair after brain injury.
Full Text of this Article in Japanese PDF (465K)

(臨床神経, 50：882−885, 2010)
key words：神経新生，免疫調整，E-セレクチン，制御性T細胞，脳梗塞

（受付日：2010年5月21日）