XXXX -capping of @entity1 T lymphocyte adhesion/activation molecules and their redistribution during interaction with endothelial cells.

@entity1 @entity32 @entity15735 @entity3138 @entity1759 @entity1196 @entity1454 @entity1453
Lymphocyte-endothelial cell interactions are mediated in part by multiple lymphocyte surface adhesion/activation molecules and their cognate ligands. We investigated the surface localization of several of these molecules implicated in T cell adhesion and transendothelial migration mechanisms to determine if spatial regulation of their distribution contributes to these processes. T lymphocyte suspensions were stained to define distribution, ability to be aggregated into energy-dependent caps, and potential cocapping of several adhesion structures. @entity3138 , @entity1759 , @entity1196 ( @entity1196 , LECCAM-1), and @entity1453 / @entity1454 ( @entity1453 ) exhibited uniform distribution on the T cell surface by direct immunofluorescence but formed caps in an energy-dependent, and therefore cytoskeletally driven, manner when examined by indirect immunofluorescence. @entity3138 was shown to @entity15735 -cap (unidirectionally cocap) with @entity1759 and @entity1453 / @entity1454 ( @entity1453 ), an observation potentially related to functional cooperation among these molecules in T cell activation. T cells were also added to endothelial cell monolayers to assess, in a physiologically relevant context, potential surface molecule reorganization. Lymphocytes co-cultured with @entity1 umbilical vein endothelial cells (HUVEC) underwent a profound shape change, from essentially round cells to polarized cells bearing pseudopodia. Immunofluorescent localization of T cell adhesion/activation molecules using confocal microscopy revealed the redistribution of @entity3138 , @entity1759 , and @entity1196 to the pseudopod. In contrast, @entity1453 / @entity1454 remained globally distributed on the cell surface, even in severely deformed cells. Both lymphocyte shape change and membrane molecule redistribution appear to be cell-cell contact-dependent phenomena requiring intact, viable endothelial cells. Mechanisms that control these events may be critical to lymphocyte recirculation and @entity32 .
