• Orie Saino, Akihiko Taguchi, Takayuki Nakagomi, Akiko Nakano-Doi, Shin-Ichiro Kashiwamura, Nobutaka Doe, Nami Nakagomi, Toshihiro Soma, Hiroo Yoshikawa, David M Stern, Haruki Okamura, and Tomohiro Matsuyama.
• Institute for Advanced Medical Sciences, Hyogo College of Medicine, Hyogo, Japan.
• J. Neurosci. Res. 2010 Aug 15; 88 (11): 2385-97.

AbstractAcute inflammation in the poststroke period exacerbates neuronal damage and stimulates reparative mechanisms, including neurogenesis. However, only a small fraction of neural stem/progenitor cells survives. In this report, by using a highly reproducible model of cortical infarction in SCID mice, we examined the effects of immunodeficiency on reduction of brain injury, survival of neural stem/progenitor cells, and functional recovery. Subsequently, the contribution of T lymphocytes to neurogenesis was evaluated in mice depleted for each subset of T lymphocyte. SCID mice revealed the reduced apoptosis and enhanced proliferation of neural stem/progenitor cells induced by cerebral cortex after stroke compared with the immunocompetent wild-type mice. Removal of T lymphocytes, especially the CD4(+) T-cell population, enhanced generation of neural stem/progenitor cells, followed by accelerated functional recovery. In contrast, removal of CD25(+) T cells, a cell population including regulatory T lymphocytes, impaired functional recovery through, at least in part, suppression of neurogenesis. Our findings demonstrate a key role of T lymphocytes in regulation of poststroke neurogenesis and indicate a potential novel strategy for cell therapy in repair of the central nervous system.(c) 2010 Wiley-Liss, Inc.

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