期刊
TRENDS IN IMMUNOLOGY
卷 38, 期 8, 页码 606-615出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.it.2017.05.002
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类别
资金
- Israel Science Foundation
- Flight Attendant Medical Research Institute Foundation (FAMRI) USA
- Minerva Foundation, Germany
- Landsteiner Foundation for Blood Transfusion Research (LSBR)
- Rembrandt Institute for Cardiovascular Research
Leukocyte transendothelial migration (TEM) takes place across micron-wide gaps in specific post-capillary venules generated by the transmigrating leukocyte. Because endothelial cells contain a dense cytoskeletal network, transmigrating leukocytes must overcome these mechanical barriers as they squeeze their nuclei through endothelial gaps and pores. Recent findings suggest that endothelial cells are not a passive barrier, and upon engagement by transmigrating leukocytes trigger extensive dynamic modifications of their actin cytoskeleton. Unexpectedly, endothelial contractility functions as a restrictor of endothelial gap enlargement rather than as a facilitator of gap formation as was previously suggested. In this review we discuss current knowledge regarding how accurately timed endothelial actin-remodeling events are triggered by squeezing leukocytes and coordinate leukocyte TEM while preserving blood vessel integrity.
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