Objective To use gene cloning techniques to construct the gene overexpression/siRNA lentiviral vector of C-type lectin receptor (CLR) and observe the effects of the overexpressed/low expressed CLR, which are on surface of placenta originated dendritic cells, on the invasion, adhesion ability, and apoptosis of extravillous cytotrophoblasts (EVCT). Methods The CLR overexpressed/low expressed dendritic cells were acquired by plasmid transfection and RNA interference. The primary human EVCT were isolated, cultured, identified and then co-cultured with CLR overexpressed/low expressed dendritic cells (i.e. the overexpressing group and low expressing group). The effects of co-culture on invasion, adhesion ability, and apoptosis of EVCT were examined by the in vitro invasion assay, adhesion experiment, and AnnexinV/PI double staining. The EVCT not being co-cultured were used as the control group. Results The differences of invasiveness of EVCT between the overexpressing group and the control group were not statistically significant (P>0.05). The invasiveness of EVCT of the low expressing group was distinctly weaker than that of the control group (P<0.01). The value of adhesive ability of the overexpressing group was (94.2±2.3)% and the value of adhesive ability of the control group and the low expressing group was only (52.8±1.5)%. The adhesive ability of EVCT of the low expressing group was significantly lower (P<0.01). The apoptotic rates of the overexpressing group, low expressing group, and control group were (3.9±0.8)%, (8.2±1.4)%, and (1.1±0.3)%, respectively. The apoptotic rate of the low expressing group was significantly higher than that of the control group (P<0.01). Conclusion To inhibit the expressing of CLR on surface of dendritic cells can significantly decrease the invasiveness and adhesion ability of EVCT and significantly increase the apoptotic rate. This indicates that the abnormal expression of CLR may be one of the important mechanisms of the immune injury of EVCT and the onset of preeclampsia.