期刊
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
卷 32, 期 4, 页码 598-611出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/jcbfm.2012.6
关键词
immune system; ischemia; neurogenesis; reperfusion; stroke; T lymphocytes
资金
- National Health and Medical Research Council of Australia [350327, APP1006017]
- Australian Research Council (ARC) [FT100100427]
- Australian Research Council [FT100100427] Funding Source: Australian Research Council
Following an ischemic stroke, T lymphocytes become activated, infiltrate the brain, and appear to release cytokines and reactive oxygen species to contribute to early inflammation and brain injury. However, some subsets of T lymphocytes may be beneficial even in the early stages after a stroke, and recent evidence suggests that T lymphocytes can also contribute to the repair and regeneration of the brain at later stages. In the hours to days after stroke, T-lymphocyte numbers are then reduced in the blood and in secondary lymphoid organs as part of a 'stroke-induced immunodeficiency syndrome,' which is mediated by hyperactivity of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis, resulting in increased risk of infectious complications. Whether or not poststroke T-lymphocyte activation occurs via an antigen-independent process, as opposed to a classical antigen-dependent process, is still controversial. Although considerable recent progress has been made, a better understanding of the roles of the different T-lymphocyte subpopulations and their temporal profile of damage versus repair will help to clarify whether T-lymphocyte targeting may be a viable poststroke therapy for clinical use. Journal of Cerebral Blood Flow & Metabolism (2012) 32, 598-611; doi:10.1038/jcbfm.2012.6; published online 1 February 2012
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