Neonatal exposure to idiotype induces Schistosoma mansoni egg antigen-specific cellular and humoral immune responses

Exposure of neonatal mice to appropriate, cross-reactive Id (CRI) preparati ons alters immune responsiveness, ameliorates pathology, and prolongs survi val of animals upon subsequent Schistosoma mansoni infection. However, beca use schistosome infections profoundly affect host immunobiology, which resp onses are effected by neonatal Id exposure alone and which responses are in fluenced by infection is unclear, To directly examine the schistosome solub le egg Ag (SEA)-specific immune responses altered by CRI exposure, neonatal mice were injected with CRT-expressing (CRI+) SEA-specific Ab preparations , SEA-specific Abs that did not express CRI (CRI-), or normal mouse Ig, At 9 wk of age, only mice that were neonatally exposed to CRI+ anti-SEA Abs di splayed significant SEA-specific IgG serum levels and spleen cell prolifera tive responses. SEA-stimulated spleen cells from these CRI+-exposed mice al so produced IFN-gamma although not at significantly higher levels than mice receiving CRI- Id or normal mouse Ig, If CRI+-exposed mice were also injec ted with SEA at 8 wk of age, the 9-wk IFN-gamma responses were significantl y higher than those of the other neonatal injection groups. The presence of both CRT and anti-CRI in the sera of animals neonatally injected with CRI, but receiving no exposure to S. mansoni Ags or infection, suggested a func tional idiotypic network led to these responses. These data demonstrate tha t appropriate idiotypic exposure induces B and T cell responsiveness to the Ag recognized by the Id and support the hypothesis that neonatal idiotypic exposure can be an important immunoregulatory factor in schistosomiasis.