For example, mucosal immune cells can respond to microbial products or antigens from the commensal microbiota by producing cytokines, and the overexpression of proinflammatory cytokines (such as IL-1, IL-2, IL-5, IL-6, IL-12, IL-18, and IFN-γ) can promote the development of IBD [33–35]. This evidence concerns the gene IL18 and inflammatory bowel disease.