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Isolates of Trichuris muris elicit different adaptive immune responses in their murine host
Author(s) -
Johnston C. E.,
Bradley J. E.,
Behnke J. M.,
Matthews K. R.,
Else K. J.
Publication year - 2005
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 - 10.1111/j.1365-3024.2005.00746.x
Subject(s) - biology , immune system , antigen , host (biology) , immunology , parasite hosting , microbiology and biotechnology , lymph node , mesenteric lymph nodes , acquired immune system , strain (injury) , trichuris , helminths , virology , genetics , anatomy , world wide web , computer science
SUMMARY The J and S isolates of Trichuris muris have different infection profiles in C57BL/6 mice; J worms are expelled, S worms survive to chronicity. Building on this, the ability of the J and S isolates to survive, and the quality of the immune response induced was explored in three different strains of mouse. The resistant BALB/c mouse mounted a strong Th2 response against both isolates, which were quickly expelled. The susceptible AKR host mounted a Th1 response and retained both isolates. Despite equivalent worm exposure, mesenteric lymph node cells from AKR mice infected with the S isolate produced significantly higher levels of IL‐12 and the intestinal mastocytosis was reduced. IgG1 and IgG2a from S‐infected AKR mice recognized low molecular weight antigens not recognized by J‐infected mice. Differential expulsion kinetics was observed in the slower‐responding C57BL/6 strain; J worms were expelled but S isolate worms were retained. Survival of the S isolate was again associated with elevated IL‐12 and decreased Th2 responses. In resistant mouse strains, the outcome of infection is thus dominantly influenced by host genetics. However, in the slower‐responding host, isolate‐derived factors may play a role in shaping the quality of the adaptive immune response, thus influencing parasite survival.