Objectives: We investigated the phenotype and functional characteristics of decidual CD1a+ and CD83+ dendritic cells stimulated with or without TAG-72 (Tumor Associated Glycoprotein 72) and their interactions with autologous decidual NK cells and T cells. Methods of the study: The first trimestar decidua of normal human pregnancy, mucosa of the fallopian tubes with ectopic implantation and away from the place of implantation, and the endometrium of women with ectopic pregnancy were obtained by collagenase digestion. We used flow cytometry to analyze the expression of phenotype, degree of activation, intracellular expression of cytokines, chemokines, binding assay and FITC–dextran andocytosis by CD1a+ or/and CD83+ dendritic cells. Magnetic sepration was used for purification of decidual subpopulations. We visualised isolated, refined decidual CD1a+ cells by immunocytochemistry. Presence and distribution of CD1a+ , CD209+ and TAG-72+ cells at the feto-maternal interface were analyzed by immunohistology. Results: Decidual CD1a+ dendritic cells have immature phenotype, due to low expression of CD83, HLA-DR and costimulatory molecules, but they express high amount of endocytic receptors (CD206 and CD209). Contrary to CD83+ cells, CD1a+ cells expressed more IL-15, IFN-γ and CD195 chemokine receptor for inflammatory chemokines. The interaction between CD1a+ cells and autologous NK cells lead to reduced expression of IL-15 and NKp46 receptor and increased expression of cytotoxic mediators in CD56+ cells. Furthermore, CD1a+ dendritic cells efficiently stimulate proliferation of CD56+ cells compared to CD83+ dendritic cells. CD56+ cells significantly killed CD83+ cells. TAG-72 was bound and internalized by carbohydrate recognition domain to CD206 and CD209 receptors expressed on CD1a+ cells in a dose dependent manner. TAG-72 in vitro decreased the expression of CD83 and CD91 molecules, IL-15, IFN-γ and CCL17, whereas it increased the expression of D6 and IL-1RII on CD1a+ dendritic cells. TAG-72 stimulated CD1a+ dendritic cells decreased the expression of IFN-γ in autologous syngenic and allogenic cells from umbilical cord blood, even in the presence of lipopolysaccharide. TAG-72 enhanced also proliferation of T cells isolated from umbilical cord blood in a dose dependent manner. Intracellular expression of IL-15 and IFN-γ in CD1a+ dendritic cells at the site of implantation and distant from implantation site in tubal pregnancy, where the TAG-72 was present, were very low, in compare to the lining of the uterus in ectopic pregnancy, where the TAG-72 missing. Conclusion: Removal of TAG-72 from feto-maternal interface, probably contributes to a better control of trophoblast invasion through NK and T cells, because it does not affect the maturation of CD1a+ cells without anti-inflammatory properties that otherwise occur when is TAG-72 present.