Open AccessHealing of intestinal inflammation by IL‐22
Author(s) -
Mizoguchi Atsushi
Publication year - 2012
Publication title -
inflammatory bowel diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.932
H-Index - 146
eISSN - 1536-4844
pISSN - 1078-0998
DOI - 10.1002/ibd.22929
Subject(s) - immunology , inflammation , proinflammatory cytokine , inflammatory bowel disease , mucus , mucin , cytokine , wound healing , biology , goblet cell , interleukin 23 , barrier function , stimulation , colitis , medicine , disease , microbiology and biotechnology , interleukin 17 , epithelium , neuroscience , pathology , ecology
An interleukin (IL)‐10 family cytokine, IL‐22 is characterized by several unique biological properties, including 1) the target restricted to innate cells; 2) the distinct expression pattern between large and small intestines; 3) alteration of the cellular source depending on several factors; 4) the dual abilities to serve as protective versus proinflammatory mediators in inflammatory responses; and 5) the close association with some major inflammatory bowel disease (IBD) susceptibility genes. The major functions of IL‐22 in the intestine are the stimulation of epithelial cells to produce a wide variety of antibacterial proteins, the reinforcement of mucus barrier through stimulation of mucin 1 production under intestinal inflammatory conditions, and the enhancement of epithelial regeneration with goblet cell restitution. Through these beneficial functions, IL‐22 contributes to the improvement of some types of experimental chronic colitis, which are mediated by T helper (Th)1 or Th2 responses. Most important, studies using both loss‐of‐function and gain‐of‐function approaches have clearly demonstrated the ability of IL‐22 to promote intestinal wound healing from acute intestinal injury. These findings highlight IL‐22 as an attractive and promising target for future IBD therapy. Alternatively, the enormous progress in the field of IL‐22 biology has also suggested more complicated mechanisms with the IL‐22 pathway than previously predicted. This review article briefly summarizes previous and current knowledge on IL‐22 particularly associated with intestinal inflammation. (Inflamm Bowel Dis 2012;)