Modulation of the cellular immune response by a carbohydrate rich fractionfrom Echinococcus granulosus protoscoleces in infected or immunized Balb/cmice

Citation
S. Dematteis et al., Modulation of the cellular immune response by a carbohydrate rich fractionfrom Echinococcus granulosus protoscoleces in infected or immunized Balb/cmice, PARASITE IM, 23(1), 2001, pp. 1-9
Citations number
30
Categorie Soggetti
Immunology
Journal title
PARASITE IMMUNOLOGY
ISSN journal
01419838 → ACNP
Volume
23
Issue
1
Year of publication
2001
Pages
1 - 9
Database
ISI
SICI code
0141-9838(200101)23:1<1:MOTCIR>2.0.ZU;2-M
Abstract
Infection of Balb/c mice with Echinococcus granulosus protoscoleces constit utes the model for secondary hydatid infection. The immune response of Balb /c mice infected with E. granulosus is characterized by secretion of antibo dies specific for carbohydrate epitopes and production of type-2 cytokines. A role for glycoconjugates in the induction of type-2 responses has been s uggested in other host-parasite systems. Although glycoconjugates are immun ogenic in E. granulosus infection, the role of these molecules in the estab lishment of the type-2 response has never been analysed. in this study, a c arbohydrate rich fraction (E4(+)) from E. granulosus protoscoleces was obta ined using the monoclonal antibody E492/G1 specific for the moiety Gal alph a (1,4)- Gal which is widely represented in protoscoleces and other E. gran ulosus antigenic preparations. The results showed that E4(+) was immunogeni c in Balb/c mice evoking an antibody response mainly directed against carbo hydrate epitopes. In addition, splenocytes from E4(+)-immunized mice showed suppressed proliferative responses to Con A and E4(+) induced IL-10 secret ion by E4(+)-primed and naive splenocytes. the fraction E4(+) also was immu nogenic in infected mice during early infection. In this case also, splenoc ytes from infected mice as well as peritoneal cells from infected or naive mice, when stimulated in vitro with E4(+), secreted IL-10. Collectively, th ese results suggest that E4(+) may be involved in immunosuppression phenome na and, by stimulating IL-10 secretion, may contribute to the induction and sustaining of the type-2 cytokine response established in early experiment al infection.