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1.
J Reprod Immunol ; 104-105: 68-79, 2014 Oct.
Article in English | MEDLINE | ID: mdl-24837231

ABSTRACT

The expression of endothelial HLA-E in the context of the systemic inflammatory response observed in preeclampsia has not been established. An experimental study was designed to determine the effect of the sera of pregnant women on the expression of HLA-E in EA.hy296 endothelial cells. First, measurements of protein fractions were performed in sera from early-onset, severely preeclamptic women without HELLP syndrome, in which there was no significant difference in total proteins between the groups, but a reduced level of plasma albumin and an increase in α1-globulin were observed in both groups of pregnant women compared with non-pregnant women. Measurements of colloid osmotic pressure (COP) using a recalculated albumin/globulin ratio formula determined only a significant decrease in COP in all pregnant groups compared with non-pregnant women. The expression of membrane HLA-E was increased in EA.hy296 endothelial cells stimulated with sera of early-onset, severely preeclamptic women, while recombinant interferon-γ (IFN-γ) significantly reduced the expression of membrane HLA-E. Pro-inflammatory cytokines were measured by Luminex in the serum samples, and increased levels of tumor necrosis factor (TNF) and decreased levels of IFN-γ were observed in early-onset, severe preeclampsia compared with normal pregnancy. Moreover, soluble HLA-E was detected in these serum samples by Western blot and ELISA, but no significant difference was found. This raises the possibility that a systemic inflammatory response promotes a compensatory mechanism of COP balance in severe preeclampsia by release of inflammation-induced factors, including endothelial HLA-E. Evidence is now provided regarding HLA-E expression by EA.hy296 cells.


Subject(s)
Endothelial Cells/metabolism , Gene Expression Regulation/drug effects , Histocompatibility Antigens Class I/biosynthesis , Pre-Eclampsia/blood , Serum , Cell Line, Tumor , Endothelial Cells/immunology , Female , Gene Expression Regulation/immunology , Histocompatibility Antigens Class I/immunology , Humans , Interferon-gamma/blood , Interferon-gamma/immunology , Pre-Eclampsia/immunology , Pregnancy , Prospective Studies , Severity of Illness Index , HLA-E Antigens
2.
J Reprod Immunol ; 97(2): 223-31, 2013 Apr.
Article in English | MEDLINE | ID: mdl-23415844

ABSTRACT

Preeclampsia involves an exacerbated maternal inflammatory response that suggests a possible role of innate immunity. NK cells can promote this kind of response through cytokine production and the expression of activating or inhibitory receptors. The aims of the present study were to explore cytokine production by peripheral blood mononuclear cells, as well as cytotoxic ability and receptor expression for HLA-E and HLA-G molecules in peripheral natural killer (NK) cells of women with early-onset severe preeclampsia without HELLP (hemolysis, elevated liver enzyme levels and a low platelet count) syndrome. The expression of the ILT2, KIRDL4, NKG2A, and NKG2C receptors and of cytotoxic activity was measured in non-stimulated NK cells, whereas the intracellular expression of IL-4, IL-10, IL-13, IL-12, IFNγ, TNF and VEGF, was assessed in non-stimulated peripheral blood mononuclear cells subsets using flow cytometry. Circulating soluble HLA-G was also determined by ELISA. The intracellular cytokines tested were significantly higher in NK cell subsets from severely preeclamptic women compared with the control group. On the other hand, the percentage of NK cells expressing NKG2A or NKG2C and the cytotoxic activity of NK cells were significantly higher in severely preeclamptic women. Furthermore, there was a significant correlation between urine protein concentration and soluble human leukocyte antigen G (soluble HLA-G) in serum. We conclude that patients with early-onset severe preeclampsia without HELLP syndrome have increased NK cell function related to cytokine production, cytotoxicity and expression of lectin-like receptors such as NKG2.


Subject(s)
Cytokines/biosynthesis , Killer Cells, Natural/immunology , Pre-Eclampsia/immunology , Adolescent , Adult , Antigens, CD/biosynthesis , Female , HELLP Syndrome , HLA-G Antigens/biosynthesis , HLA-G Antigens/blood , Histocompatibility Antigens Class I/biosynthesis , Humans , Inflammation/immunology , Killer Cells, Natural/metabolism , Leukocyte Immunoglobulin-like Receptor B1 , Leukocytes, Mononuclear/immunology , Leukocytes, Mononuclear/metabolism , Lymphocyte Count , NK Cell Lectin-Like Receptor Subfamily C/biosynthesis , Pre-Eclampsia/blood , Pregnancy , Receptors, Immunologic/biosynthesis , Receptors, KIR/biosynthesis , Young Adult , HLA-E Antigens
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