Published online Aug 7, 2010. doi: 10.3748/wjg.v16.i29.3638
Revised: April 22, 2010
Accepted: April 29, 2010
Published online: August 7, 2010
In the gut of patients with Crohn’s disease and patients with ulcerative colitis, the major forms of inflammatory bowel diseases (IBD) in humans, the tissue-damaging immune response is mediated by an active cross-talk between immune and non-immune cells. Accumulating evidence indicates also that cytokines produced by these cells play a major role in initiating and shaping this pathologic process. One such cytokine seems to be interleukin (IL)-21, a member of the common γ-chain-receptor family. IL-21 is produced in excess in the inflamed intestine of patients with IBD mostly by activated CD4+ T helper cells co-expressing interferon-γ and follicular T helper cells. Moreover, both in vitro and in vivo studies indicate that excessive IL-21 production leads to the activation of multiple signaling pathways that expand and sustain the ongoing mucosal inflammation. In this article, we review the available data supporting the pathogenic role of IL-21 in IBD.