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Parasitol Res. 2003 Aug;90(5):415-20. Epub 2003 May 16.

Angiostrongylus costaricensis infection in C57BL/6 mice: MHC-II deficiency results in increased larval elimination but unaltered mortality.

Author information

1
Institut für Tropenmedizin, Universität Tübingen, Wilhelmstrasse 27, 72074, Tübingen, Germany. stefan.geiger@tropa.vetmed.uni-muenchen.de

Abstract

During experimental Angiostrongylus costaricensis infections in several inbred mouse strains, genetic factors as well as different cytokine secretion patterns have recently been shown to play a role in the outcome of infection in terms of morbidity and mortality, e.g. BALB/c mice show a high and C57BL/6 mice a low mortality during the acute phase of infection. In this study, C57BL/6 MHC-II knockout mice infected with A. costaricensis did not show increased mortality during the acute phase of infection when compared with wild-type mice. Furthermore, MHC-II knockout mice showed a strongly diminished parasite-specific humoral and cellular immune response, which can be explained by the nearly complete lack of CD4+ T cells in the periphery. This defect in MHC-II genes, the lack of CD4+ T cells, and the resulting cellular and humoral unresponsiveness resulted in a three times higher output of first-stage larvae in feces compared with wild-type animals. The results indicate that during experimental A. costaricensis infection a parasite-specific immune response, directed via MHC-II molecules and CD4+ T cells, is not essential for the survival of C57BL/6 mice during the acute phase of infection, whereas the elimination of first-stage larvae seems to be regulated by a MHC-II- and CD4+ T-cell-dependent mechanism.

PMID:
12750994
DOI:
10.1007/s00436-003-0853-2
[Indexed for MEDLINE]

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