XXXX endothelial cells induce and regulate cytolytic T cell differentiation.

@entity1 @entity137 @entity14638 @entity379 @entity405
We compared the capacity of cultured @entity1 endothelial cells (EC) vs B lymphoblastoid cells ( @entity14638 ) from the same donor to stimulate allogeneic @entity405 + T cells to differentiate into CTL, assaying for @entity137 , T cell growth, @entity379 secretion, and perforin expression. The input cell number affected specificity and potency of the resulting CTL. At low input (<10(5) cells/ well), anti-EC CTL were rarely detected. At high input (>10(6) cells/well), anti-EC CTL developed that displayed unrestricted, low-titer killing and an unstable phenotype. At intermediate input (1.0-2.5 x 10(5) cells/well), classical class I MHC-restricted, @entity405 +, and perforin-positive anti-EC CTL developed with reproducible frequencies. However, under all conditions EC were less efficient stimulators than @entity14638 from the same donor. Anti-EC CTL did not kill @entity14638 , whereas anti- @entity14638 CTL killed @entity14638 and EC from the same donor with comparable efficiency. When @entity405 + T lymphocytes were grown in the presence of EC and @entity14638 together, the differentiation of anti- @entity14638 CTL was completely suppressed, while the anti-EC response was intact. The inhibition of the allogeneic anti- @entity14638 CTL response was independent of T cell-EC contact, and proliferation of @entity405 + T cells was inhibited by EC-conditioned medium. We conclude that EC are competent but less efficient activators of CTL differentiation than are @entity14638 and that EC actively regulate differentiation and/or expansion of allospecific CTL.
