Regulatory T cells from @entity694 @entity1 express @entity13796 and inhibit transendothelial effector T cell migration by an XXXX -dependent mechanism.

@entity1 @entity859 @entity5 @entity8582 @entity694 @entity13796 @entity356 @entity855
UNASSIGNED: T cell-mediated immunity is a major component of anti- @entity5 immunity. In order to be efficient, effector T cells must leave the circulation and enter into the @entity5 tissue. We have shown that regulatory T cells (Treg) from @entity356 @entity1 , but not from healthy volunteers, potently inhibit migration of conventional T cells through activated endothelium. In this study, we compared T cells from @entity694 @entity1 and healthy donors to determine the mechanisms used by Treg from @entity5 @entity1 to inhibit conventional T cell migration. Our results showed that circulating Treg from @entity5 @entity1 expressed high levels of @entity13796 , an ectoenzyme mediating hydrolysis of @entity855 to @entity8582 , as a rate-determining first step in the generation of immunosuppressive @entity859 . Tumor-associated Treg expressed even more @entity13796 , and we therefore examined the importance of @entity859 in Treg-mediated inhibition of T cell transendothelial migration in vitro. Exogenous @entity859 significantly reduced migration of conventional T cells from healthy volunteers, and blocking of @entity859 receptors or @entity13796 activity during transmigration restored the ability of conventional T cells from @entity5 @entity1 to migrate. @entity859 did not directly affect T cells or endothelial cells, but reduced the ability of monocytes to activate the endothelium. Taken together, our results indicate that Treg-derived @entity859 act on monocytes and contribute to reduced transendothelial migration of effector T cells into @entity5 . This effect of Treg is specific for @entity5 @entity1 , and our results indicate that Treg may not only affect T cell effector functions but also their migration into @entity5 .
