Although this immunomodulation could be driven by the presence of other stressors such as pollutants (87–89) or other concurrent but undetected infectious disease interfering with the immunological response and exacerbating a high parasite burden, the effect of treatment on expression of IL-6 suggests that the suppression of IL-6 and the subsequent dampening of the anti-parasitic T-helper 2 response is at least partly hookworm-driven, as is the case in hookworm infections in humans (90, 91). Here, IL6 is linked to infectious disease.