Neonatal idiotypic exposure alters subsequent cytokine, pathology, and survival patterns in experimental Schistosoma mansoni infections

Exposure to maternal idiotypes (Ids) or antigens might predispose a child t o develop an immunoregulated, asymptomatic clinical presentation of schisto somiasis. We have used an experimental murine system to address the role of Ids in this immunoregulation. Sera from mice with 8-wk Schistosoma mansoni infection, chronic (20-wk infection) moderate splenomegaly syndrome (MSS), or chronic hypersplenomegaly syndrome (HSS) were passed over an S. mansoni soluble egg antigen (SEA) immunoaffinity column to prepare Ids (8WkId, MSS Id, HSS Id). Newborn mice were injected with 8WkId, MSS Id, HSS Id, or nor mal mouse immunoglobulin (NoMoIgG) and infected with S. mansoni 8 wk later. Mice exposed to 8WkId or MSS Id as newborns had prolonged survival and dec reased morbidity compared with mice that received HSS Id or NoMoIgG. When s timulated with SEA, 8WkId, or MSS Id, spleen cells from mice neonatally inj ected with 8WkId or MSS Id produced more interferon gamma than spleen cells from mice neonatally injected with HSS Id or NoMoIgG. Furthermore, neonata l exposure to 8WkId or MSS Id, but not NoMoIgG or HSS Id, led to significan tly smaller granuloma size. and lower hepatic fibrosis levels in infected m ice. Together, these results indicate that perinatal exposure to appropriat e anti-SEA Ids induces long-term effects on survival, pathology, and immune response patterns in mice subsequently infected with S. mansoni.