期刊
JOURNAL OF NEUROSCIENCE RESEARCH
卷 88, 期 11, 页码 2385-2397出版社
WILEY
DOI: 10.1002/jnr.22410
关键词
adult stem cells; apoptosis; cerebral cortex; ischemia; inflammation; lymphocyte; neural stem cells; CD4(+) T cell
资金
- JSPS [18234567]
- Hyogo College of Medicine
- Mitsubishi Pharma Research Foundation
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [22730593] Funding Source: KAKEN
Acute 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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