Since the MyD88-mediated pathway plays a key role in IL-1R signaling [3], unimpaired IL-1β–induced TNF-α and IL-6 production by macrophages from helminth-infected host suggests that the effect of the helminth infection is not on MyD88-dependent signals, but is likely to be on the TRAM/TRIF pathway. Here, TNF is linked to helminthiasis.