IL‐1‐dependent,IL‐1R1‐independent resistance to gastrointestinal nematodes

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‐1α and IL‐1β 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 naïve 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.