Activated platelets are the source of elevated levels of soluble @entity2936 ligand in the circulation of XXXX @entity1 .

@entity1 @entity32 @entity1356 @entity2936 @entity31 @entity11603 @entity23079 @entity29 @entity30 @entity1361
BACKGROUND: The @entity2936 / @entity11603 system, a key regulator and amplifier of immune reactivity, is activated in @entity29 ( @entity29 ) mucosa. AIMS: To determine whether plasma levels of sCD40L are elevated in @entity30 ( @entity30 ) and @entity31 ( @entity31 ) @entity1 compared with normal controls, to investigate the cellular source of sCD40L, and to explore @entity11603 induction mechanisms. @entity1 : @entity30 , @entity31 , and normal control subjects were studied. METHODS: The concentration of sCD40L in plasma and supernatants of freshly isolated platelets and autologous peripheral blood T cells (PBT) was measured by ELISA. Surface @entity11603 expression level was measured by flow cytometry in resting and thrombin activated platelets, and unstimulated and CD3/ @entity1361 stimulated PBT before and after coculture with @entity1 intestinal microvascular endothelial cells (HIMEC). RESULTS: Compared with normal controls, plasma sCD40L levels were significantly higher in both @entity30 and @entity31 @entity1 and proportional to the extent of @entity32 . Platelets from @entity29 @entity1 displayed a significantly higher surface @entity11603 expression than those from control subjects, and released greater amounts of sCD40L than autologous @entity23079 . Contact with @entity1356 activated HIMEC induced significant upregulation of @entity11603 surface expression and release by platelets. CONCLUSIONS: Elevated levels of sCD40L in the circulation of @entity29 @entity1 reflect enhanced surface expression and release of @entity11603 by platelets. This phenomenon translates to an increased platelet activation state apparently induced by passage through an inflamed mucosal microvascular bed, a conclusion supported by the positive correlation of plasma sCD40L levels with the extent of anatomical involvement by @entity29 . These results suggest that platelet-endothelial interactions critically contribute to activation of the @entity2936 pathway in @entity29 .
