Literature DB >> 8641783

Induction of differential T-helper-cell responses in mice infected with variants of the parasitic nematode Trichuris muris.

T Bellaby1, K Robinson, D Wakelin.   

Abstract

The resistance or susceptibility of mice to infection with the intestinal nematode parasite Trichuris muris is closely correlated with polarization of T helper (Th) cell responses to the type 2 (Th2) or type 1 (Th1) subset. Comparison of infections with three isolates of T. muris (E/K, E/N, and S) in three inbred strains of mice (CBA, C57BL/10, and B10.BR) has shown that host Th response phenotype can be parasite determined. Although the mouse strains used show genetically determined variation in ability to respond to T. muris (CBA > C57BL/10 > B10.BR), the speed of worm expulsion in a given strain depended upon the isolate used for infection (E/K > E/N > S). The two isolates that induced the most effective resistance (E/K and E/N) elicited parasite-specific host antibody responses that were dominated by immunoglobulin G1 (IgG1), and antigen-stimulated T cells from infected mice released interleukin-5 in vitro. With the isolate that induced the least host resistance (S), the dominant antibody response was IgG2a, and T cells released gamma interferon in vitro. These data show clearly that parasite variant-specific factors play a major role in Th subset polarization during infection.

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Year:  1996        PMID: 8641783      PMCID: PMC173839          DOI: 10.1128/iai.64.3.791-795.1996

Source DB:  PubMed          Journal:  Infect Immun        ISSN: 0019-9567            Impact factor:   3.441


  22 in total

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Authors:  K J Else; R K Grencis
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4.  Cellular immune responses to the murine nematode parasite Trichuris muris. II. Differential induction of TH-cell subsets in resistant versus susceptible mice.

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Journal:  Immunology       Date:  1992-02       Impact factor: 7.397

5.  The worm and the protozoa: stereotyped responses or distinct antigens?

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  11 in total

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9.  Expulsion of Trichuris muris is associated with increased expression of angiogenin 4 in the gut and increased acidity of mucins within the goblet cell.

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