Previous reports have associated these effects with a variety of mechanisms such as increased adipose tissue content of eosinophils [37,40,63], ILC2 infiltration [37], M2 polarization [35,36,40], PPARγ activation [35,64], increased expression of IL33 [65], and microbiota modulation [66] indicating that helminth infection might employ a variety of mechanisms to influence metabolic syndrome, especially inducing type 2 immune response polarization which should counter regulate the obesity-associated inflammation with high levels of IL6 [25], IFNγ [25], TNF [67], IL1ß [68] and CCL2 [69]. The gene discussed is IL33; the disease is obesity due to melanocortin 4 receptor deficiency.