炎症
CD44细胞
肺
细胞外基质
受体
免疫学
细胞粘附分子
医学
癌症研究
细胞生物学
病理
生物
细胞
内科学
生物化学
作者
Priit Teder,R. William Vandivier,Dianhua Jiang,Jiurong Liang,Lauren Cohn,Ellen Puré,Peter M. Henson,Paul W. Noble
出处
期刊:Science
[American Association for the Advancement of Science]
日期:2002-04-05
卷期号:296 (5565): 155-158
被引量:680
标识
DOI:10.1126/science.1069659
摘要
Successful repair after tissue injury and inflammation requires resolution of the inflammatory response and removal of extracellular matrix breakdown products. We have examined whether the cell-surface adhesion molecule and hyaluronan receptor CD44 plays a role in resolving lung inflammation. CD44-deficient mice succumb to unremitting inflammation following noninfectious lung injury, characterized by impaired clearance of apoptotic neutrophils, persistent accumulation of hyaluronan fragments at the site of tissue injury, and impaired activation of transforming growth factor-beta1. This phenotype was partially reversed by reconstitution with CD44+ cells, thus demonstrating a critical role for this receptor in resolving lung inflammation.
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