However, the fact that—in contrast to what was observed in inflammasome-deficient mice [33]—there was no reduction in total IL-1β levels in livers of Dectin-2−/− mice during S. mansoni infection would suggest that, downstream of Dectin-2, the PGE2-OX40L axis rather than inflammasome activation plays a key role in Th2 priming during, and in the immunopathological outcome of, this infection. This evidence concerns the gene TNFSF4 and infection.