Journal
NATURE IMMUNOLOGY
Volume 12, Issue 8, Pages 761-U145Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2062
Keywords
-
Categories
Funding
- Wellcome Trust [081172/Z/06/Z]
- UK National Institute for Health Research
- Swiss National Science Foundation [310000-122423, 310000-109402, CR32I3_129987, 310030- 120184]
- Juvenile Diabetes Research Foundation [40-2011-11]
- European Union [BETAIMAGE 222980, IMIDIA, C2008-T7, FP7-PEOPLE-2009-IEF-252091]
- US National Institutes of Health
- National Cancer Institute
- Deutsche Forschungsgemeinschaft
- Wellcome Trust [081172/Z/06/Z] Funding Source: Wellcome Trust
- Swiss National Science Foundation (SNF) [310030-120184] Funding Source: Swiss National Science Foundation (SNF)
Ask authors/readers for more resources
The migration of neutrophils into inflamed tissues is a fundamental component of innate immunity. A decisive step in this process is the polarized migration of blood neutrophils through endothelial cells (ECs) lining the venular lumen (transendothelial migration (TEM)) in a luminal-to-abluminal direction. By real-time confocal imaging, we found that neutrophils had disrupted polarized TEM ('hesitant' and 'reverse') in vivo. We noted these events in inflammation after ischemia-reperfusion injury, characterized by lower expression of junctional adhesion molecule C (JAM-C) at EC junctions, and they were enhanced by blockade or genetic deletion of JAM-C in ECs. Our results identify JAM-C as a key regulator of polarized neutrophil TEM in vivo and suggest that reverse TEM of neutrophils can contribute to the dissemination of systemic inflammation.
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