Journal
MEDIATORS OF INFLAMMATION
Volume 2015, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2015/946509
Keywords
-
Categories
Funding
- Mexican Council for Science and Technology [Conacyt: 179895, 207268, 233395]
- American Heart Association [AHA GIA 13GRNT 14560068]
- National Institutes of Health [NIH HL097406, HL123658]
- Arthritis Research UK [19913]
- Dutch Heart Foundation [2005T039]
- LSBR foundation [1701]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R44HL097406, R43HL097406, R01HL123658] Funding Source: NIH RePORTER
- Versus Arthritis [19913] Funding Source: researchfish
Ask authors/readers for more resources
Leukocyte extravasation is one of the essential and first steps during the initiation of inflammation. Therefore, a better understanding of the key molecules that regulate this process may help to develop novel therapeutics for treatment of inflammation-based diseases such as atherosclerosis or rheumatoid arthritis. The endothelial adhesion molecules ICAM-1 and VCAM-1 are known as the central mediators of leukocyte adhesion to and transmigration across the endothelium. Engagement of these molecules by their leukocyte integrin receptors initiates the activation of several signaling pathways within both leukocytes and endothelium. Several of such events have been described to occur during transendothelial migration of all leukocyte subsets, whereas other mechanisms are known only for a single leukocyte subset. Here, we summarize current knowledge on regulatory mechanisms of leukocyte extravasation from a leukocyte and endothelial point of view, respectively. Specifically, we will focus on highlighting common and unique mechanisms that specific leukocyte subsets exploit to succeed in crossing endothelial monolayers.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available