Zahr, AlisarAlcaide, PilarYang, JinlingJones, AlexanderGregory, Meredithdela Paz, Nathaniel G.Patel-Hett, SunitaNevers, TaniaKoirala, AdarshaLuscinskas, FrancisSaint-Geniez, MagaliKsander, BruceD'Amore, PatriciaArgueso, Pablo2016-04-012016Zahr, A., P. Alcaide, J. Yang, A. Jones, M. Gregory, N. G. dela Paz, S. Patel-Hett, et al. 2016. “Endomucin prevents leukocyte–endothelial cell adhesion and has a critical role under resting and inflammatory conditions.” Nature Communications 7 (1): 10363. doi:10.1038/ncomms10363. http://dx.doi.org/10.1038/ncomms10363.2041-1723http://nrs.harvard.edu/urn-3:HUL.InstRepos:26318644Endomucin is a membrane-bound glycoprotein expressed luminally by endothelial cells that line postcapillary venules, a primary site of leukocyte recruitment during inflammation. Here we show that endomucin abrogation on quiescent endothelial cells enables neutrophils to adhere firmly, via LFA-1-mediated binding to ICAM-1 constitutively expressed by endothelial cells. Moreover, TNF-α stimulation downregulates cell surface expression of endomucin concurrent with increased expression of adhesion molecules. Adenovirus-mediated expression of endomucin under inflammatory conditions prevents neutrophil adhesion in vitro and reduces the infiltration of CD45+ and NIMP-R14+ cells in vivo. These results indicate that endomucin prevents leukocyte contact with adhesion molecules in non-inflamed tissues and that downregulation of endomucin is critical to facilitate adhesion of leukocytes into inflamed tissues.en-USJournal Article2016-04-0110.1038/ncomms10363