Objective To investigate the impacts of mannan- binding lectin( MBL) on the phenotype and function of CD11c- positive human peripheral blood myeloid dendritic cells( CD11c+m DC). Methods CD11c+m DC and CD4+T lymphocytes from healthy human volunteers were isolated by magnetic bead sorting and were stimulated by different concentrations of MBL( 5,10,20 μg/ml). Compared with the non- MBL stimulation group,the levels of interleukin- 12( IL- 12) in the supernatant of culture medium in different MBL stimulation groups were determined by enzyme- linked immunosorbent assay( ELISA). The expression of CD40,CD80,CD86,and HLA- DR on CD11c+m DC surface was measured by flow cytometry. CD11c+m DC- stimulated proliferation abilities of CD4+T lymphocytes were determined by MTT assay. The levels of interleukin- 4( IL- 4) and interferon- gamma( IFNγ) in the coculture medium were measured by ELISA. Comparison of the means between multiple groups was made by one- way ANOVA and pairwise comparison between any two groups was made by LSD t- test. Results Compared with the non- MBL stimulation group,the MBL stimulation groups( 5,10,20 μg/ml) had significantly higher expression of CD40,CD80,CD86,and HLA- DR on CD11c+m DC surface and significantly increased IL- 12 secretion( F = 44. 34,P < 0. 001; F = 27. 35,P < 0. 001; F = 15. 57,P < 0. 001; F = 48. 38,P < 0. 001; F = 38. 27,P < 0. 001). The IL- 12 secretion was MBL concentration- dependent. The proliferation ability of CD4+T lymphocytes was significantly higher in the MBL stimulation group than in the non- MBL stimulation group and the control group( F = 23. 43,P < 0. 001). The MBL group had a significantly higher IFNγ level but a significantly lower IL- 4 level compared with the non- MBL group and the control group( F = 28. 25,P < 0. 001; F =40. 03,P < 0. 001). Conclusion MBL can effectively stimulate the activation of CD11c+m DC and induce the differentiation from CD4+T lymphocytes to type 1 helper T cells. Therefore,MBL is possibly involved in the control and clearance of hepatitis B virus by regulating the phenotype and function of CD11c+m DC.