Interleukin 22 (IL-22) was identified in 2000 as an IL-10 related cytokine that signals through class II cytokine receptor proteins (1). IL-22 signaling is different from IL-10 since some cell lines respond to IL-22 by activatingSTAT(Signal Transducer and Activator of Transcription) proteins, but are unresponsive to IL-10 (1). The counterpart of human IL-22 in mouse is called IL-TIF(3). Il-22 functions through IL-22 receptor (IL-22R), and a common IL-10R2 receptor that is shared by other members of the IL-10 family (2). A natural antagonist of IL-22, IL-22 binding protein, was found to down-regulate IL-22 function (4). IL-22 is produced by dendritic cells, T-cells and natural killer cells during bacterial infection, auto-immunity and tissue inflammation (6, 7). IL-22 acts upon innate immunity cells through its receptors expressed exclusively on these cells. In CD4+ T helper cells, IL-22 expression has been found to be associated with Th17 and Th1. Recently, an IL-22 expressing T helper cell subset (Th22) was characterized (10) which is distinct from other T cells by coexpression of the chemokine receptorCCR6 and the skin-homing receptorsCCR4 andCCR10. IL-22 expression is elevated in psoriatic skin inflammation (5, 8, 11, 12), atopic dermatitis (13), inflammatory bowel disease (14). In cutaneous T-cell lymphoma, IL-22 dominates the tumor microenvironment andSTAT3 phosphorylation was observed (17). IL-22 was also found to promote murine hepatocyte survival (16) and ameliorate intestinal inflammation in mouse ulcerative colitis model (9).