While the general consensus is that IL-4 acts as a canonical Th2 cytokine to induce a detrimental Th2/type 2 response, there have been studies demonstrating that early production of IL-4 at the site of infection may essentially drive a beneficial Th1 response, under the instruction of DCs secreting IL-12 (11, 100, 101). This evidence concerns the gene IL4 and infection.