engleski

Mucine 1 hampers the proliferation and the cytolytic mediators' expression in NK cells sustained by CD14+ antigen presenting cells at the maternal-fetal interface

Mucine 1 (MUC 1) is removed from the surface of uterine mucosa at the time of successful implantation, but the immunological reasons for its disappearance are not completely understood. We explored in vitro the influence of MUC 1 on the properties of normal early pregnancy decidual CD14+ cells and their interaction with cognate NK cells. MUC I in the suspension of isolated decidual mononuclear cells binds and internalizes carbohydrate recognition domain of CD206 on CD14+ cells on a dose dependent manner. MUC 1 did not significantly change the expression of co stimulatory molecules, HLA-DR, decoy receptors, IFN-, IL-4, CCL3, CCL17 and CCL22, as it was detected by flow cytometry. The percentage and mean fluorescence intensity for IL-15 decreased in MUC 1 treated CD14+ cells in comparison to untreated cells. MUC 1 treated CD14+ cells less efficiently proliferate magnetically purified decidual CD56+ cells in 48 hours CFSE proliferation assay. These cells were unable to sustain perforin and Fas ligand cytotoxic proteins expression in CD56+ cells after 18 hours co-culture, in comparison to untreated cells. MUC 1 was not detected by B72.3 monoclonal antibody used in immunohistology of paraffin embedded first trimester uterine decidua of normal and pathological pregnancies, whereas MUC 1 was present in tubal mucosa of ectopic pregnancy. The appearance of MUC 1 was negatively correlated with the tissue accumulation of CD56+ NK cells. All these data suggest that MUC 1, if present at the maternal- fetal interface, might decrease IL-15 expression in tissue specific CD14+ cells which could not sustain proliferation and cytolytic mediators’ expression in mucosal CD56+ cells. Acknowledgement: The experiments were financed by Croatian Ministry of Science, Grants No. 0620402-0376, No. 062-620402-0377 and 0620402- 0379.

Mucin 1; NK cells; maternal-fetal interface

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