For example, it promotes cytokine production by intestinal epithelial cells and monocytes [22], increases the production of Tumor Necrosis Factor α, (TNFα), Interleukin 2 (IL-2), Interleukin 6 (IL-6), and Interferon-γ (IFNγ) in a cold-stress and infection model [33] and elicits Interleukin 1β (IL-1β) from monocytes that, in turn, drive T-helper 1 (Th1) and T-helper 17 (Th17) responses [34]. This evidence concerns the gene IL2 and infection.