In early stages of active infection, Th1 cellular immune responses are protective, as interferon gamma (IFNγ) and interleukin 12 (IL-12) induce macrophage activation, allowing bacterial growth control; nevertheless, during late active disease, extensive inflammation leads to a shift toward a Th-2 immune response in which IL-4, IL-10, and transforming growth factor-β (TGF-β) induce a local anti-inflammatory and immunosuppressive milieu resulting in poor containment of infection and progression of tissue damage, necrosis, and fibrosis, driving host to death (6). This evidence concerns the gene IL10 and infection.