Immunological Aspects of Acute StrokeTherapeutic Implications
作者:
Thomas J. DeGraba,
期刊:
BioDrugs
(ADIS Available online 2000)
卷期:
Volume 13,
issue 1
页码: 1-8
ISSN:1173-8804
年代: 2000
出版商: ADIS
关键词: Immune function;Reviews on disease;Stroke, pathogenesis
数据来源: ADIS
摘要:
Recent studies strongly suggest that cerebral ischaemia initiates a focal inflammatory response that results in significant secondary injury to brain tissue, thereby extending the ultimate size of a stroke. Factors involved in this cascade include the release of cytokines that cause a pro-inflammatory and prothrombotic state on cerebral vessel endothelium, the expression of leucocyte adhesion molecules, and the release of chemotactic factors allowing the migration of leucocytes into the area of injured brain tissue causing further damage. Animal studies have clearly demonstrated the detrimental effects of these inflammatory mediators in stroke models and additionally have shown dramatic reduction in infarct size using leucocyte adhesion modification and cytokine receptor blockade. The approach of modifying the effects of inflammatory cytokines and/or limiting leucocyte adhesion and migration into the region of injury holds great promise for identifying agents that will give significant neuronal protection following a stroke.
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