Since the participant children have probably experienced repeated STH infections since they were much younger, their immune response may have already changed to a modified Type 2 response, where inflammatory Th2 shifted to an attenuated phenotype characterized by the shutdown of effector cytokines such as IL-5, retention of IL-4, and reinforcement of anti-inflammatory cytokines such as IL-10 and/or TGF-β [4, 9]. This evidence concerns the gene TGFB1 and infection.