Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 39, Issue 4, Pages 1036-1045Publisher
WILEY
DOI: 10.1002/eji.200838938
Keywords
Cytokine; Infection; Parasitic-helminth; Proinflammatory; T cells
Categories
Funding
- Medical Research Council (MRC) [71672]
- Wellcome Trust [064820]
- MRC [G0400737] Funding Source: UKRI
- Medical Research Council [G0400737] Funding Source: researchfish
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IL-1 null mice are unable to expel the intestinal nematode Trichuris muris; whereas WT littermates exhibit sterile immunity. Intriguingly the essential signalling components IL-1R1 and IL-1R accessory protein (AcP) are dispensable for expulsion of this parasite. IL-1 is thus critical for CD4(+) Th2-mediated immunity to T. muris; however, this action is independent of the established IL-1 signalling receptor. We also present data demonstrating that both IL-1 alpha and IL-1 beta induce measurable effects on T. muris primed cells isolated from IL-1R1 or IL-1R AcP null mice. MLN cells from these mice restimulated with parasite antigen proliferated at a greater rate and produced more cytokines in response to exogenous IL-1. This ability to respond to IL-1 was restricted to these parasite-primed cells and importantly was not evident in cells from naive gene null mice. These in vitro data are consistent with the observed ability of mice with compromised IL-1 signalling to expel the parasite, bolstering the premise that an alternative IL-1 signalling mechanism is accessible in the context of an intestinal helminth-driven Th2 immune response.
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