Published online Dec 28, 2014. doi: 10.3748/wjg.v20.i48.18177
Revised: June 21, 2014
Accepted: September 5, 2014
Published online: December 28, 2014
Inflammatory bowel disease (IBD) is a chronic inflammatory disease thought to be mediated by the microbiota of the intestinal lumen and inappropriate immune responses. Aberrant immune responses can cause secretion of harmful cytokines that destroy the epithelium of the gastrointestinal tract, leading to further inflammation. Interleukin (IL)-22 is a member of the IL-10 family of cytokines that was recently discovered to be mainly produced by both adaptive and innate immune cells. Several cytokines and many of the transcriptional factors and T regulatory cells are known to regulate IL-22 expression through activation of signal transducer and activator of transcription 3 signaling cascades. This cytokine induces antimicrobial molecules and proliferative and antiapoptotic pathways, which help prevent tissue damage and aid in its repair. All of these processes play a beneficial role in IBD by enhancing intestinal barrier integrity and epithelial innate immunity. In this review, we discuss recent progress in the involvement of IL-22 in the pathogenesis of IBD, as well as its therapeutic potential.
Core tip: Interleukin (IL)-22 is expressed by adaptive immune system cells and innate lymphocytes. Several cytokines and many transcriptional factors and T regulatory cells can regulate IL-22 expression. Through activation of signal transducer and activator of transcription 3 signaling cascades, IL-22 induces antimicrobial, proliferative and antiapoptotic pathways, which can help fix damaged tissue and promote tissue repair mechanisms. IL-22 is also associated with inflammatory bowel disease (IBD) susceptibility genes that regulate inflammatory responses in tissues. All of these processes play crucial roles in IBD pathogenesis and collectively provide an important rationale for the development of novel therapeutic measures for this disease.