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Modulation of the cellular immune response by a carbohydrate rich fraction from Echinococcus granulosus protoscoleces in infected or immunized Balb/c mice

生物 表位 免疫系统 平衡/c 细粒棘球绦虫 脾细胞 糖复合物 抗原 免疫学 抗体 单克隆抗体 生物化学 动物
作者
Sylvia Dematteis,Fiorella Pirotto,João Pedro Marques,Alberto Nieto,Anders Örn,Adriana Baz
出处
期刊:Parasite Immunology [Wiley]
卷期号:23 (1): 1-9 被引量:55
标识
DOI:10.1046/j.1365-3024.2001.00346.x
摘要

Infection of Balb/c mice with Echinococcus granulosus protoscoleces constitutes the model for secondary hydatid infection. The immune response of Balb/c mice infected with E. granulosus is characterized by secretion of antibodies specific for carbohydrate epitopes and production of type‐2 cytokines. A role for glycoconjugates in the induction of type‐2 responses has been suggested in other host–parasite systems. Although glycoconjugates are immunogenic in E. granulosus infection, the role of these molecules in the establishment of the type‐2 response has never been analysed. In this study, a carbohydrate rich fraction (E4 + ) from E. granulosus protoscoleces was obtained using the monoclonal antibody E492/G1 specific for the moiety Galα(1,4)Gal which is widely represented in protoscoleces and other E. granulosus antigenic preparations. The results showed that E4 + was immunogenic in Balb/c mice evoking an antibody response mainly directed against carbohydrate epitopes. In addition, splenocytes from E4 + ‐immunized mice showed suppressed proliferative responses to Con A and E4 + induced IL‐10 secretion by E4 + ‐primed and naive splenocytes. The fraction E4 + also was immunogenic in infected mice during early infection. In this case also, splenocytes from infected mice as well as peritoneal cells from infected or naive mice, when stimulated in vitro with E4 + , secreted IL‐10. Collectively, these results suggest that E4 + may be involved in immunosuppression phenomena and, by stimulating IL‐10 secretion, may contribute to the induction and sustaining of the type‐2 cytokine response established in early experimental infection .
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