Among these are IL-4 and IL-13 resulting in the alternative activation of macrophages [16], prostaglandin D2, which cleaves IL-33 resulting in increased type 2 innate lymphoid cell induction through CRTH2 receptor interaction [17], and TNF-α, CXCL1 and CXCL2 leading to the recruitment and proliferation of neutrophils at the site of infection [18,19]. This evidence concerns the gene IL33 and infection.