| Abstract: | Chronic murine schistosomiasis is characterized by a host cell-mediated immune response to schistosomal egg antigens. This response is manifested in vitro by lymphocyte blastogenic reactivity to a soluble schistosomal egg antigen preparation (SEA) and in vivo by delayed dermal hypersensitivity to SEA. In addition, mice develop reaginic, agglutinating, and early dermal reactive antibodies to SEA and a characteristic pattern of peripheral blood eosinophilia. In this study, depletion of thymus-dependent lymphocytes abolished the anti-SEA lymphocyte blastogenic response and delayed dermal reactivity, reaginic antibody response and the major peak of peripheral blood eosinophilia, which in normal mice occurs at the same time as SEA-induced blastogenesis. Antibodies mediating the early dermal reaction to SEA and agglutinins for SEA-coated particles were not inhibited by T-lymphocyte depletion. The experimental group did not develop the normally observed granulomatous response, but rather suffered focal hepatic and mucosal liquefactive necrosis, bacteremia and accelerated mortality. |
