| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3355529 | Immunology Letters | 2013 | 8 Pages |
•IL-27 inhibits the production of IL-22 in CD4+ T cells from CBMCs.•The suppression of IL-22 is not dependent on the production of IFN-γ and IL-10.•IL-27 promotes the expression of SOCS1.•The expression of IL-22 could not be inhibited with the lower expression of SOCS1.•IL-27 inhibits the production of IL-22 in naive and memory CD4+ T cells from PBMCs.
IL-27, a member of IL-6/IL-12 cytokine family, plays pro- and anti-inflammatory functions in immune responses. It can promote inflammation by inducing Th1 differentiation and exert the inhibitory effects on Th2 and Th17 mediated immune responses. Moreover, IL-27 suppresses CD28-mediated IL-2 production from mouse naive CD4+ T cells. In the present study, we demonstrate that IL-27 inhibits the production of IL-22 and induces the expression of IFN-γ in CD4+ T cells from human umbilical cord blood mononuclear cells (CBMCs) stimulated with anti-CD3 and anti-CD28 in dose-dependent manner. In addition, the suppression of IL-22 is not dependent on the production of IFN-γ and IL-10. Importantly, IL-27 promotes the expression of SOCS1, which could be inhibited by a Jak2/STAT inhibitor, AG490. Importantly, the expression of IL-22 could not be inhibited under the circumstances with the lower expression of SOCS1. Moreover, IL-27 inhibits the production of IL-22 in CD4+CD45RA+ and CD4+CD45RO+ T cells from PBMCs. These data identify that IL-27 may suppress the production of IL-22 by inducing the expression of SOCS1 in human CD4+ T cells. Furthermore, it demonstrates that IL-27 may be a therapeutic approach in the treatment of IL-22-mediated diseases.
