WSX-1:a key role in induction of chronic intestinal nematode infection

Bancroft, Allison J. and Humphreys, Neil E. and Worthington, John J. and Yoshida, Hiroki and Grencis, Richard K. (2004) WSX-1:a key role in induction of chronic intestinal nematode infection. Journal of Immunology, 172 (12). pp. 7635-7641. ISSN 0022-1767

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Abstract

Chronic infection by the gastrointestinal nematode Trichuris muris in susceptible AKR mice, which mount a Th1 response, is associated with IL-27p28 expression in the cecum. In contrast to wild-type mice, mice that lack the WSX-1/IL-27R gene fail to harbor a chronic infection, having significantly lower Th1 responses. The lower level of Ag-specific IFN-gamma-positive cells in WSX-1 knockout (KO) mice was found to be CD4(+) T cell specific, and the KO mice also had increased levels of IL-4-positive CD4(+) T cells. Polyclonal activation of mesenteric lymph node cells from naive WSX-1 KO or wild-type mice demonstrated that there was no inherent defect in the production of IFN-gamma by CD4(+) T cells, suggesting the decrease in these cells seen in infected WSX-1 KO mice is an in vivo Ag-driven effect. IL-12 treatment of WSX-1 KO mice failed to rescue the type 1 response, resulting in unaltered type-2-driven resistance. Infection of WSX-1 KO mice was also associated with a reduction of IL-27/WSX-1 downstream signaling gene expression within the cecum. These studies demonstrate an important role for WSX-1 signaling in the promotion of type 1 responses and chronic gastrointestinal nematode infection.

Item Type:
Journal Article
Journal or Publication Title:
Journal of Immunology
Uncontrolled Keywords:
/dk/atira/pure/subjectarea/asjc/2700
Subjects:
?? ANIMALSCECUMCHRONIC DISEASEGENE EXPRESSION REGULATIONINTERFERON-GAMMAINTERLEUKIN-12INTESTINAL DISEASES, PARASITICLYMPHOCYTE COUNTMICEMICE, KNOCKOUTNEMATODE INFECTIONSRECEPTORS, CYTOKINESIGNAL TRANSDUCTIONTH1 CELLSTRICHURIASISMEDICINE(ALL) ??
ID Code:
78929
Deposited By:
Deposited On:
04 Apr 2016 08:44
Refereed?:
Yes
Published?:
Published
Last Modified:
18 Sep 2023 00:59