Premium
Diminished immunopathology in Schistosoma mansoni infection following intranasal administration of cholera toxin B‐immunodominant peptide conjugate correlates with enhanced transforming growth factor‐β production by CD4 T cells
Author(s) -
Hernandez Hector J.,
Rutitzky Laura I.,
Lebens Mike,
Holmgren Jan,
Stadecker Miguel J.
Publication year - 2002
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1046/j.1365-3024.2002.00482.x
Subject(s) - biology , schistosoma mansoni , cholera toxin , immunology , antigen , epitope , t cell , immune system , immunogenicity , schistosomiasis , virology , microbiology and biotechnology , helminths
Summary In Schistosoma mansoni infection, CD4 T cells specific for parasite egg antigens mediate perioval granuloma formation in the liver and intestines. Mice of the CBA strain develop a severe form of disease and a significant proportion of their CD4 T cell response is directed against the major egg antigen Sm‐p40 and its immunodominant T cell epitope peptide 234–246. Here, we show that intranasal (i.n.) treatment of infected CBA mice with a fusion protein of the cholera toxin B subunit (CTB) with peptide 234–246 (CTB::pep) results in significant down‐modulation of hepatic granulomatous inflammation and fibrosis. Moreover, egg antigen‐stimulated dispersed hepatic granuloma cells, as well as mesenteric lymph node CD4 T cells from the CTB::pep‐treated mice, produced significantly more transforming growth factor (TGF)‐β than that produced by treated or untreated controls. The data demonstrate that i.n. administration of a single immunodominant peptide conjugated to CTB can lead to down‐regulation of the hepatic immunopathology associated with schistosomiasis, and that this down‐regulation is, at least in part, mediated by TGF‐β.