Maternal Immune Responses to the Fetus in Human Pregnancy

Sargent, Ian L.; Redman, Christopher W.G.

doi:10.1007/978-94-009-1247-2_5

Cited by 31 publications

(37 citation statements)

References 111 publications

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“…This "modification" of the immune system during pregnancy, which may be called "immunosuppression" or "tolerance" and allows the survival of the fetus within the maternal uterus, was proposed some years ago [25,35]. The activated immune system of the pregnant mice, as triggered by adoptive cell transfer, may act specifically at the feto-maternal interface, reinforcing the natural but scarce maternal immunity due to the presence of the allogeneic fetus [36,37]. Additionally, it is possible that the Th1 cytokines secreted by transferred immune cells induce the further infiltration of macrophages or other antigen-presenting cells, which prime cytotoxic T cells to paternal antigens that are expressed by fetal cells [37].…”

Section: Discussionmentioning

confidence: 99%

Introducing a mouse model for pre‐eclampsia: adoptive transfer of activated Th1 cells leads to pre‐eclampsia‐like symptoms exclusively in pregnant mice

et al. 2004

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Pre-eclampsia (PE) is the most severe pregnancy-related disease, leading to high maternal and fetal morbidity/mortality. Immunological imbalances associated with endothelial cell dysfunction have been hypothesized as a cause for the onset and perpetuation of PE. Valid and reliable animal models are urgently required to test this hypothesis and to better understand the mechanisms underlying PE. We developed a novel PE-model by adoptively transferring activated BALB/c Th1-like splenocytes into allogeneically pregnant BALB/c female mice during late gestation; the model mimicked the symptoms of PE, i.e. increased blood pressure and glomerulonephritis accompanied by proteinuria. Interestingly, these PE-like symptoms were not detectable in non-pregnant recipients of activated Th1-like cells. Adoptive cell transfer adversely affected the outcome of pregnancy by increasing fetal rejection, with uterine immune cells showing an inflammatory profile. In conclusion, we have established a valid and reliable PE mouse model, which opens vast opportunities for therapeutic interventions.

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Section: Discussionmentioning

confidence: 99%

Introducing a mouse model for pre‐eclampsia: adoptive transfer of activated Th1 cells leads to pre‐eclampsia‐like symptoms exclusively in pregnant mice

et al. 2004

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“…Despite being biological allografts, fetuses are not normally rejected by the maternal immune system [1]. One likely explanation for this phenomenon is that the feto-placental unit is an immunologically privileged site that creates a mechanical barrier that reduces interactions between fetal tissues and maternal lymphocytes [2], and/or functionally impairs the maternal immune response [3]. Earlier studies have focused on the modifications of the immunological response characteristic of pregnancy.…”

Section: Introductionmentioning

confidence: 99%

“…Twenty-four hours later, the cultures were pulsed with 1 Ci 3 Hthymidine, and harvested after 18 h using a 96-well cell harvester (TOMTEC Inc., Orange, CT). 3 H determinations were made using an LKB Beta-plate spectrometer (Pharmacia LKB Biotechnology, Piscataway, NJ). The method used to calculate IL-2 units has previously been described [26].…”

mentioning

confidence: 99%

Characterization of type 1 and type 2 cytokine production profile in physiologic and pathologic human pregnancy

Marzi

Viganò²,

Trabattoni

et al. 1996

Clinical and Experimental Immunology

566

380

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SUMMARYAntigen-and mitogen-stimulated cytokine production by peripheral blood mononuclear cells (PBMC) of 50 pregnant women and 31 age-and sex-matched non-pregnant controls were analysed to determine whether changes in cytokine production occur during normal and pathologic human gestation. The pregnant women, consecutively enrolled during a 3-month period, were undergoing a normal, nonpathologic pregnancy at the time of entry into the study, and underwent ultrasound examination to ascertain the exact week of pregnancy and the vitality of the fetus. Forty of the 50 pregnancies (80%) terminated physiologically with the birth of normal babies. Spontaneous abortions were observed in 5/50 (10%) women, and five women gave birth to newborns small for gestational age (SGA). A decrease in the production of IL-2 and interferon-gamma (IFN-°) accompanied by an increase in production of IL-4 and IL-10, was observed in normal pregnancy, with the lowest quantities of IL-2 and IFN-°and the highest quantities of IL-4 and IL-10 present in the third trimester of pregnancy. Statistically significant increased production of both IL-2 and IFN-°and reduced production of IL-10 characterized pathologic pregnancies and distinguished them from normal pregnancies. These preliminary data suggest that a type 2 cytokine profile may be associated with normal human pregnancy, whereas the lack of a dominant type 2 cytokine profile may be indicative of a pathologic pregnancy.

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“…The placenta provides a barrier between the mother and child, preventing maternal immune cells from entering the fetal compartment at a time when its own immune system is immature or absent. Trophoblast cells of the placenta invade deep into the maternal uterine tissue to establish a life-giving connection with the maternal blood supply (1). HLA-G has long been assumed a major factor in this immune accommodation because of its localized expression and because of low levels of allelic polymorphism (2,3).…”

mentioning

confidence: 99%

Protein Expression and Peptide Binding Suggest Unique and Interacting Functional Roles for HLA-E, F, and G in Maternal-Placental Immune Recognition

Ishitani

Sageshima

Lee

et al. 2003

The Journal of Immunology

314

276

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In this study we focused on the structure and expression of the HLA-E, F, and G class I complexes in placental tissue. Structural analysis included an examination of the peptides bound to soluble and membrane forms of the HLA-G complex isolated directly from placenta. An important distinction was observed from HLA-G bound peptides previously isolated from transfectant cells. Thus, the number of distinct moieties bound to placental-derived proteins was substantially lower than that bound to transfectant-derived HLA-G. Indeed, a single peptide species derived from a cytokine-related protein alone accounted for 15% of the molar ratio of HLA-G bound peptide. To further examine HLA-E and its potential to bind peptide, notably that derived from HLA-G, we combined new Abs to examine expression in placental tissues for all the known forms of the nonclassical class I molecules. Whereas membrane HLA-G was found in extravillous trophoblasts, soluble HLA-G was found in all placental trophoblasts, including villous cytotrophoblasts and syncitiotrophoblasts. Further, HLA-E was found in all cells that expressed either form of HLA-G, consistent with HLA-E being complexed with the HLA-G signal sequence-derived nonamer in these cells. Finally, using new reagents specific for HLA-F, a restricted pattern of expression was observed, primarily on extravillous trophoblasts that had invaded the maternal decidua. Comparative staining indicated that HLA-F was on the surface of these cells, defining them as the first to demonstrate surface expression of this Ag and the first cell type identified to express all three nonclassical HLA class I Ags simultaneously.

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Maternal Immune Responses to the Fetus in Human Pregnancy

Cited by 31 publications

References 111 publications

Introducing a mouse model for pre‐eclampsia: adoptive transfer of activated Th1 cells leads to pre‐eclampsia‐like symptoms exclusively in pregnant mice

Introducing a mouse model for pre‐eclampsia: adoptive transfer of activated Th1 cells leads to pre‐eclampsia‐like symptoms exclusively in pregnant mice

Characterization of type 1 and type 2 cytokine production profile in physiologic and pathologic human pregnancy

Protein Expression and Peptide Binding Suggest Unique and Interacting Functional Roles for HLA-E, F, and G in Maternal-Placental Immune Recognition

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