| First Author | Zenewicz LA | Year | 2008 |
| Journal | Immunity | Volume | 29 |
| Issue | 6 | Pages | 947-57 |
| PubMed ID | 19100701 | Mgi Jnum | J:142640 |
| Mgi Id | MGI:3821896 | Doi | 10.1016/j.immuni.2008.11.003 |
| Citation | Zenewicz LA, et al. (2008) Innate and adaptive interleukin-22 protects mice from inflammatory bowel disease. Immunity 29(6):947-57 |
| abstractText | Inflammatory bowel disease (IBD) is a chronic inflammatory disease thought to be mediated by dysfunctional innate and/or adaptive immunity. This aberrant immune response leads to the secretion of harmful cytokines that destroy the epithelium of the gastrointestinal tract and thus cause further inflammation. Interleukin-22 (IL-22) is a T helper 17 (Th17) T cell-associated cytokine that is bifunctional in that it has both proinflammatory and protective effects on tissues depending on the inflammatory context. We show herein that IL-22 protected mice from IBD. Interestingly, not only was this protection mediated by CD4+ T cells, but IL-22-expressing natural killer (NK) cells also conferred protection. In addition, IL-22 expression was differentially regulated between NK cell subsets. Thus, both the innate and adaptive immune responses have developed protective mechanisms to counteract the damaging effects of inflammation on tissues. |
