title: Specific decidual CD14(+) cells hamper cognate NK cell proliferation and cytolytic mediator expression after mucin 1 treatment in vitro.
abstract: Mucin 1 (MUC1) forms a glycocalyx on the surface of decidual epithelial cells that needs to be removed for successful embryo attachment. We investigated whether MUC1 affects human early pregnancy decidual CD14(+) cells and their interactions with cognate decidual natural killer (NK) cells. FITC-dextran internalisation, surface and intracellular antigen levels, and proliferation of CD14(+) and/or CD56(+) cells were analysed by flow cytometry. Magnetic separation was used to purify CD56(+) and CD14(+) cells. Uncultured CD14(+) cells expressed a negligible percentage of CD1a and CD83 molecules. They expressed lower levels of CD16, and higher levels of endocytic mannose receptors (MR), dendritic cell-specific intercellular adhesion molecule grabbing non-integrin (DC-SIGN), proinflammatory chemokine CC receptor 5 (CCR5), and CD163 receptor, than their peripheral blood counterparts. Lipopolysaccharide stimulation did not affect FITC-dextran internalisation in CD14(+) cells. MUC1 bound and internalised, in a dose-dependent manner, the carbohydrate recognition domain of MR, increasing the decoy IL-1 receptor type II and decreasing IL-15 expression in CD14(+) cells. In the presence of MUC1-treated macrophages, the expression levels of the proliferation and cytotoxic mediators (perforin, Fas ligand and TNF-related activation-induced ligand or TRAIL) was attenuated, while that of the anti-inflammatory chemokine CCL17 was increased, in NK cells compared with untreated macrophages. In conclusion, MUC1 supports the alternative activation of tissue-specific CD14(+) cells, and may restrict proliferation of NK cells and regulate their content of cytotoxic mediators. Based on the experiments with first-trimester decidual cells in vitro, we conclude that removing MUC1 from decidual tissue might help control trophoblast invasion by NK cells.
authors: Department of Physiology and Immunology, University of Rijeka, 51000 Rijeka, B. Branchetta 20, Croatia. gordana.laskarin@medri.hr
authors: Gordana
authors: G
authors: Laskarin
authors: Suzana Srsen
authors: SS
authors: Medancic
authors: Arnela
authors: A
authors: Redzovic
authors: Danijel
authors: D
authors: Duric
authors: Daniel
authors: D
authors: Rukavina
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000276:immunology / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects*; D003656:Decidua / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D004847:Epithelial Cells / Q000166:cytology / Q000276:immunology; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects / Q000276:immunology; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism; D018950:Lipopolysaccharide Receptors / Q000096:biosynthesis / Q000276:immunology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000166:cytology / Q000276:immunology / Q000378:metabolism; D018396:Mucin-1 / Q000276:immunology / Q000378:metabolism / Q000494:pharmacology*; D011247:Pregnancy / Q000276:immunology* / Q000378:metabolism; D011261:Pregnancy Trimester, First / Q000276:immunology* / Q000378:metabolism; D019713:Receptors, CCR5 / Q000276:immunology / Q000378:metabolism; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000276:immunology / Q000378:metabolism; D014327:Trophoblasts / Q000166:cytology / Q000276:immunology / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; C060192:MUC1 protein, human; D018396:Mucin-1; D019713:Receptors, CCR5; D053221:TNF-Related Apoptosis-Inducing Ligand; C505653:TNFSF10 protein, human