The inverse relationship between helminth infection and overt allergic reactivity has intrigued medical scientists for three decades. In the past 5 years, detailed epidemiological studies coupled with new experimental model approaches, have substantiated the negative effects of infection on allergic disease manifestation, and begun to provide mechanistic explanations for this fascinating interaction. Several key conclusions can now be drawn. First, the modulation of allergies, such as Th2-dependent pathologies, is not primarily through immune deviation (e.g. switching responsiveness to Th1), as helminth infections themselves drive strong Th2 responses. Second, helminth-infected hosts show similar levels of immune sensitisation to allergens as do uninfected counterparts, but the expression of overt allergic reactivity is suppressed. Third, the down-modulation of allergy in both human and experimental infections is consistent with the activity of T regulatory (Treg) cell populations, which suppress effector mechanisms of both Th1 and Th2 type.