Open AccessInterleukin-21 triggers effector cell responses in the gut
Author(s) -
Daniela De Nitto,
Massimiliano Sarra,
Francesco Pallone,
Giovanni Monteleone
Publication year - 2010
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v16.i29.3638
Subject(s) - immunology , immune system , ulcerative colitis , inflammatory bowel disease , cytokine , inflammation , biology , interleukin 23 , interleukin 22 , t helper cell , interleukin , t cell , medicine , disease , pathology
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 gamma-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-gamma 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.