The Intracellular Sensor NOD2 Induces MicroRNA-29 Expression in Human Dendritic Cells to Limit IL-23 Release

摘要: NOD2 is an intracellular sensor that contributes to immune defense and inflammation. Here we investigated whether mediates its effects through control of microRNAs (miRNAs). miR-29 expression was upregulated in human dendritic cells (DCs) response signals, regulated the multiple mediators. In particular, downregulated interleukin-23 (IL-23) by targeting IL-12p40 directly IL-23p19 indirectly, likely via reduction ATF2. DSS-induced colitis worse miR-29-deficient mice was associated with elevated IL-23 T helper 17 signature cytokines intestinal mucosa. Crohn's disease (CD) patient DCs expressing NOD2 polymorphisms failed induce upon pattern recognition receptor stimulation showed enhanced release on exposure adherent invasive E. coli. Therefore, suggest loss miR-29-mediated immunoregulation CD might contribute this disease.