title: Cytokine production by non-stimulated peripheral blood NK cells and lymphocytes in early-onset severe pre-eclampsia without HELLP.
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.
authors: Reproduction Group, School of Medicine, Universidad de Antioquia, Medellín, Colombia. jcesarbs@gmail.com
authors: J C
authors: JC
authors: Bueno-Sánchez
authors: B
authors: B
authors: Agudelo-Jaramillo
authors: L F
authors: LF
authors: Escobar-Aguilerae
authors: A
authors: A
authors: Lopera
authors: A P
authors: AP
authors: Cadavid-Jaramillo
authors: G
authors: G
authors: Chaouat
authors: J G
authors: JG
authors: Maldonado-Estrada
mesh_terms: D000293:Adolescent; D000328:Adult; D015703:Antigens, CD / Q000096:biosynthesis; D016207:Cytokines / Q000096:biosynthesis*; D005260:Female; D017359:HELLP Syndrome; D059951:HLA-G Antigens / Q000096:biosynthesis / Q000097:blood; D015395:Histocompatibility Antigens Class I / Q000096:biosynthesis; D006801:Humans; D007249:Inflammation / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology* / Q000378:metabolism; D000075362:Leukocyte Immunoglobulin-like Receptor B1; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism; D018655:Lymphocyte Count; D055654:NK Cell Lectin-Like Receptor Subfamily C / Q000096:biosynthesis; D011225:Pre-Eclampsia / Q000097:blood / Q000276:immunology*; D011247:Pregnancy; D011971:Receptors, Immunologic / Q000096:biosynthesis; D054340:Receptors, KIR / Q000096:biosynthesis; D055815:Young Adult; D000097625:HLA-E Antigens
chemical_list: D015703:Antigens, CD; D016207:Cytokines; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I; D000075362:Leukocyte Immunoglobulin-like Receptor B1; D055654:NK Cell Lectin-Like Receptor Subfamily C; D011971:Receptors, Immunologic; D054340:Receptors, KIR; D000097625:HLA-E Antigens; C527059:KLRC2 protein, human; C105299:LILRB1 protein, human