Objective      To study the role of signal transducer and activator of transcription 3 (STAT3) signaling pathway in interleukin (IL)-6-induced C-C chemokine receptor type 7 (CCR7) suppression in human monocyte-derived dendritic cells (moDCs).       Methods      To obtain human moDCs

monocytes were isolated from venous blood of healthy donor by magnetic beads coated with anti-CD14 antibody

and cultured in complete culture medium containing rhGM-CSF and recombinant human IL-4. Lipopolysaccharide (LPS) was added into the culture medium of moDCs to induce the CCR7 expression. The expression of CCR7 mRNA in the moDCs treated with different concentrations of IL-6 and then LPS was analyzed by real-time PCR. The expression of STAT3 and p-STAT3 in moDCs treated with IL-6 and moDCs treated with IL-6 and JSI-124 (selective inhibitor of STAT3 pathway) were detected by Western blotting. The expressions of CCR7 mRNA and protein in the moDCs treated with IL-6

JSI-124 and LPS were analyzed by real-time PCR and flow cytometry

respectively. The migration ability of moDCs was analyzed by Trasnwell migration experiment.       Results      Compared with the moDCs incubated with LPS only

the moDCs cultured in the presence of IL-6 expressed lower levels of CCR7 mRNA (P0.05). The expression level of p-STAT3 in the moDCs treated with LPS and IL-6 was much higher than that in the moDCs treated with LPS only. JSI-124 could significantly inhibit STAT3 hyperactivity caused by IL-6

and after STAT3 hyperactivity was inhibited with JSI-124

the CCR7 expression and migration ability of the moDCs were increased (P0.05).       Conclusion      IL-6-STAT3 pathway is involved in IL-6-induced CCR7 suppression of human moDCs

and the intervention of STAT3 pathway may be potential means for repairing the damaged cell migration of dendritic cells.