CD31 signals confer immune privilege to the vascular endothelium
dc.contributor.author | Cheung, K. | |
dc.contributor.author | Ma, L. | |
dc.contributor.author | Wang, G. | |
dc.contributor.author | Coe, D. | |
dc.contributor.author | Ferro, R. | |
dc.contributor.author | Falasca, Marco | |
dc.contributor.author | Buckley, C. | |
dc.contributor.author | Mauro, C. | |
dc.contributor.author | Marelli-Berg, F. | |
dc.date.accessioned | 2017-01-30T12:13:39Z | |
dc.date.available | 2017-01-30T12:13:39Z | |
dc.date.created | 2015-10-29T04:10:07Z | |
dc.date.issued | 2015 | |
dc.identifier.citation | Cheung, K. and Ma, L. and Wang, G. and Coe, D. and Ferro, R. and Falasca, M. and Buckley, C. et al. 2015. CD31 signals confer immune privilege to the vascular endothelium. Proceedings of the National Academy of Sciences. 112 (43): pp. E5815-E5824. | |
dc.identifier.uri | http://hdl.handle.net/20.500.11937/19397 | |
dc.identifier.doi | 10.1073/pnas.1509627112 | |
dc.description.abstract |
Maintenance of vascular integrity during effector immune responses occurring in tissues is a prerequisite of a healthy immune response. The mechanism whereby the vascular endothelium remains undamaged while interacting with effector immune cells migrating to the site of inflammation is largely unknown. This study shows that signals mediated by CD31, a trans-homophilic receptor expressed at high levels by the endothelium, are both necessary and sufficient to prevent inflammation-induced endothelial cell death and confer immune privilege to the vascular endothelium. We also provide proof of principle that this property can be harnessed therapeutically in pancreatic β-cell transplantation, whereby CD31 gene transfer alone endows allogeneic targets with indefinite resistance to immune attack in vivo. | |
dc.title | CD31 signals confer immune privilege to the vascular endothelium | |
dc.type | Journal Article | |
dcterms.source.title | Proceedings of the National Academy of Sciences | |
curtin.department | School of Biomedical Sciences | |
curtin.accessStatus | Open access via publisher |