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Neonatal Exposure to Idiotype Induces Schistosoma mansoni Egg Antigen-Specific Cellular and Humoral Immune Responses

M. Angela Montesano^*,, Daniel G. Colley, George L. Freeman, Jr. and W. Evan Secor^1,

^* Departamento de Microbiologia, Immunologia e Parasitologia, Universidade Federal de Juiz de Fora, Juiz de Fora, Minas Gerais, Brazil; and Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Public Health Service, U.S. Department of Health and Human Services, Atlanta, GA 30341

Exposure of neonatal mice to appropriate, cross-reactive Id (CRI) preparations alters immune responsiveness, ameliorates pathology, and prolongs survival of animals upon subsequent Schistosoma mansoni infection. However, because schistosome infections profoundly affect host immunobiology, which responses are effected by neonatal Id exposure alone and which responses are influenced by infection is unclear. To directly examine the schistosome soluble egg Ag (SEA)-specific immune responses altered by CRI exposure, neonatal mice were injected with CRI-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 displayed significant SEA-specific IgG serum levels and spleen cell proliferative responses. SEA-stimulated spleen cells from these CRI⁺-exposed mice also produced IFN-, although not at significantly higher levels than mice receiving CRI^- Id or normal mouse Ig. If CRI⁺-exposed mice were also injected with SEA at 8 wk of age, the 9-wk IFN- responses were significantly higher than those of the other neonatal injection groups. The presence of both CRI and anti-CRI in the sera of animals neonatally injected with CRI, but receiving no exposure to S. mansoni Ags or infection, suggested a functional idiotypic network led to these responses. These data demonstrate that 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.

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