Impacts of mannan-binding lectin on phenotype and function of CD11c-positive human peripheral blood myeloid dendritic cells

ObjectiveTo investigate the impacts of mannan-binding lectin (MBL) on the phenotype and function of CD11c-positive human peripheral blood myeloid dendritic cells (CD11c+mDC). MethodsCD11c+mDC 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+mDC surface was measured by flow cytometry. CD11c+mDC-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. ResultsCompared 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+mDC 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). ConclusionMBL can effectively stimulate the activation of CD11c+mDC 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+mDC