Description: IL-22, also known as IL-10-related T-cell derived inducible factor, is an alpha helical cytokine and is considered a member of the IFN-IL-10 family, which includes IL-19, IL-20, IL-24, IL-26, IL-28, IL-29, and the type I and II interferons. IL-22 is produced mainly by activated T and NK cells. No other immune cells (resting or activated) or non-immune cells have been found to produce IL-22. Amongst the T cells, in mice Th1 and Th17 cells appear to be the primary producers of IL-22. IL-22 acts by engaging the heterodimeric receptor complex consisting of primary receptor IL-22R1 and accessory receptor IL-10R2. IL-22R1 also binds IL-20 and IL-24; IL-10R2 also binds IL-10, IL-27, IL-28, and IL-29. Binding of IL-22 to its receptor complex induces signal transduction, particularly via the JAK-STAT pathway. In addition to the cell surface IL-22R1/IL-10R2 complex, a soluble single chain IL-22 receptor termed IL-22BP has been found to antagonize IL-22 binding and signaling. IL-22 appears not to directly influence immune cells; major targets of the cytokine appear to be nonimmune cells, such as cells of the skin, digestive and respiratory system, as well as hepatocytes, and keratinocytes.
IL-22 has been described as an effector cytokine of the Th17 lineage. Along with IL-17A and IL-17F, IL-22 regulates genes associated with innate immunity of the skin. IL-17A, IL-17F and IL-22 are all coexpressed by Th17 cells, however, differentially regulated. Note that TGFb, which is required for IL-17A production, inhibits IL-22 production. The effects of IL-22 include induction of acute phase reactants and antimicrobial proteins, as well as increasing the mobility of keratinocytes. IL-22 has been reported to mediate IL-23-induced acanthosis and dermal inflammation through activation of STAT3.