H. pylori infection culminates in high levels of TGF-β and low levels of IL-17 and IL-22 on IBD. It also induces the differentiation of Tregs and the polarization of the M1 macrophage into M2 macrophage lineage. And the ability of H. pylori neutrophil-activating protein to reduce Th2 activity may be a possible explanation for the improvement of IBD. This evidence concerns the gene IL22 and inflammatory bowel disease.