The complement system is activated in the vasculature during @entity715 and inflammatory conditions. Activation may be associated with chronic @entity32 on the endothelial surface leading to complement deposition. Complement mutations allow uninhibited complement activation to occur on platelets, neutrophils, monocytes, and aggregates thereof, as well as on red blood cells and endothelial cells. Furthermore, complement activation on the cells leads to the shedding of cell derived-microvesicles that may express complement and tissue factor thus promoting @entity32 and @entity715 . Complement deposition on red blood cells triggers hemolysis and the release of red blood cell-derived microvesicles that are prothrombotic. Microvesicles are small membrane vesicles ranging from 0.1 to 1  m, shed by cells during activation, injury and/or apoptosis that express components of the parent cell. Microvesicles are released during inflammatory and vascular conditions. The repertoire of inflammatory markers on endothelial cell-derived microvesicles shed during @entity32 is large and includes complement. These circulating microvesicles may reflect the ongoing inflammatory process but may also contribute to its propagation. This overview will describe complement activation on blood and endothelial cells and the release of microvesicles from these cells during @entity1381 , @entity2106 and @entity1333 , clinical conditions associated with enhanced @entity715 and @entity32 .

Complement Interactions with Blood Cells, Endothelial Cells and Microvesicles in XXXX and Inflammatory Conditions.

@entity32 :: ('MESH:D007249', 'Disease') :: ['inflammation'] @entity1333 :: ('MESH:D014657', 'Disease') :: ['vasculitis'] @entity1381 :: ('MESH:D006463', 'Disease') :: ['hemolytic uremic syndrome'] @entity715 :: ('MESH:D013927', 'Disease') :: ['thrombosis', 'thrombotic'] @entity2106 :: ('MESH:D011697', 'Disease') :: ['thrombotic thrombocytopenic purpura']
@entity715 :: (MESH:D013927,Disease) :: ['Thrombotic']
