Premium
Immunodeficiency reduces neural stem/progenitor cell apoptosis and enhances neurogenesis in the cerebral cortex after stroke
Author(s) -
Saino Orie,
Taguchi Akihiko,
Nakagomi Takayuki,
NakanoDoi Akiko,
Kashiwamura Shinichiro,
Doe Nobutaka,
Nakagomi Nami,
Soma Toshihiro,
Yoshikawa Hiroo,
Stern David M.,
Okamura Haruki,
Matsuyama Tomohiro
Publication year - 2010
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.22410
Subject(s) - neurogenesis , neural stem cell , progenitor cell , stem cell , biology , population , subventricular zone , neuroscience , cerebral cortex , immunology , microbiology and biotechnology , medicine , environmental health
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. © 2010 Wiley‐Liss, Inc.