Antigen presentation by human microvascular endothelial cells triggers ICAM-1-dependent transendothelial protrusion by, and fractalkine-dependent transendothelial …

TD Manes, JS Pober - The Journal of Immunology, 2008 - journals.aai.org
TD Manes, JS Pober
The Journal of Immunology, 2008journals.aai.org
TCR engagement on adherent human effector memory CD4+ T cells by TNF-treated
HUVECs under flow induces formation of a transendothelial protrusion (TEP) by the T cell
but fails to induce transendothelial migration (TEM). In contrast, TCR engagement of the
same T cell populations by TNF-treated human dermal microvascular cells (HDMEC) not
only induces TEP formation, but triggers TEM at or near the interendothelial cell junctions via
a process in which TEP formation appears to be the first step. Transduction of adhesion …
Abstract
TCR engagement on adherent human effector memory CD4+ T cells by TNF-treated HUVECs under flow induces formation of a transendothelial protrusion (TEP) by the T cell but fails to induce transendothelial migration (TEM). In contrast, TCR engagement of the same T cell populations by TNF-treated human dermal microvascular cells (HDMEC) not only induces TEP formation, but triggers TEM at or near the interendothelial cell junctions via a process in which TEP formation appears to be the first step. Transduction of adhesion molecules in unactivated HDMEC and use of blocking Abs as conducted with TNF-activated HDMEC indicate that ICAM-1 plays a nonredundant role in TCR-driven TEP formation and TEM, and that TCR-driven TEM is also dependent upon fractalkine. TEP formation, dependence on ICAM-1, and dependence on fractalkine distinguish TCR-induced TEM from IP-10-induced TEM. These in vitro observations suggest that presentation of Ag by human microvascular endothelial cells to circulating CD4+ effector memory T cells may function to initiate recall responses in peripheral tissues.
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