Intravascular fibrin deposits, hepatic infarcts and thrombocytopenia in parent/F mouse chimeras with host-versus-graft syndrome

Abstract

Host-versus-graft (HVG) disease is the fatal result of the allogenic reaction which occurs in parental strain mice perinatally inoculated with F(1) hybrid spleen cells. The principal manifestations of the syndrome in RFM/(T(6) X RFM)F(1) mice are thrombocytopenia, intestinal hemorrhage, hepatic necrosis, lymphoproliferative disorders and renal disease due to immune complexes. The discovery of intravascular fibrin deposits in the present studies establishes disseminated intravascular coagulation (DIC) as an intermediary mechanism of HVG disease. It is suggested that the characteristic declines in blood platelet levels, intestinal hemorrhages and hepatic infarcts are triggered principally by immune complexes. Cellular infiltrates of the liver, granulocytosis and hypergammaglobulinemia are other abnormalities which are regularly found in HVG mice and which are also thought to predispose to DIC.