第51回日本神経学会総会
＜シンポジウム06―2＞脳血管障害治療の次のブレークスルーを目指して
脳虚血におけるT 細胞の役割
七田 崇1)2), 此枝 史恵1)3), 吉村 昭彦1)
1）慶應義塾大学医学部微生物学免疫学教室〔〒160―8582 東京都新宿区信濃町35〕
2）九州大学大学院医学研究院病態機能内科
3）慶應義塾大学医学部神経内科
Recently, inflammation has been implicated in the progression of cerebral ischemic injury. Especially, T lymphocytes have been shown to infiltrate into the ischemic brain 24 hours after the onset, however, the function and specific subpopulation of these infiltrated T lymphocytes have not been fully understood. By using cytokine-deficient mice with transient focal ischemia model, we have shown that IL-23 and IL-17 but not IL-6 or IFN-γ play pivotal roles in the ischemic brain injury. We found that IL-23, which was mainly produced from infiltrated macrophages, induced IL-17-producing T lymphocytes in the ischemic brain. IL-23 and IL-17 expression increased 1 day or 3 day after ischemic injury, respectively, and promoted inflammatory responses by increasing the expression of neurotoxic factors. To our surprise, IL-17 was mainly produced by γδT lymphocytes, but not helper T cells. Based on these findings, we have tried to develop new therapeutic strategy for the progression of brain infarction. We found that administration of FTY720 (Fingolimod) and antibody against γδT lymphocytes attenuated ischemic brain damage. Furthermore, antibody against p40 which neutralizes both IL-23 and IL-12 simultaneously was also effective. Therefore, anti-cytokine therapy will be applicable for neuroprotection in the delayed phase of brain ischemia.
Full Text of this Article in Japanese PDF (317K)
(臨床神経, 50：878−880, 2010)
key words：脳虚血，T細胞，IL-23，IL-17， γδT細胞
（受付日：2010年5月21日）
