We found in all three contexts that TLR4 was required for robust expression of eosinophilic inflammation and airway hyperresponsiveness, but interestingly was not required for Th2 and IgE responses [25], indicating that in these contexts, TLR4 was essential to the induction of the innate component of the global type 2 immune response, but not the adaptive side controlled by Th2, Th17 and B cells. This evidence concerns the gene IGHE and airway hyperresponsiveness.