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Abstract: Pregnancy induces priming of the maternal cellular and humoral immune systems. The paternally-inherited fetal antigens that influence maternal T and B cells include both major and minor histocompatibility antigens – the same antigens that are problematic in allotransplantation. Animal models have facilitated our understanding of the lymphocyte responses to fetal antigens, and our appreciation of the parallel response in pregnant women is increasing. The physiologic properties of the placenta as well as trafficking of cells between mother and fetus allow ample opportunity for sampling of fetal proteins by the maternal immune system. Here, the current state of knowledge of fetal antigen-specific lymphocyte responses in pregnancy is reviewed. [Copyright &y& Elsevier]

Background: IgE in cord blood is thought to be a product of the fetus. A high level of total IgE is therefore used as a measure of atopic propensity in the newborn. We recently found strong evidence that allergen-specific IgE in cord blood was the result of transfer of maternal IgE to fetal blood or cord blood (maternofetal transfer) rather than fetal production. This also suggests that total IgE in cord blood might primarily be a maternal product. Objective: We sought to determine to what extent increased levels of total IgE in cord blood is the result of maternofetal transfer of IgE. Methods: Total IgE in cord blood was analyzed in a prospective birth cohort study. Maternofetal transfer of IgE was detected by means of high-sensitivity analyses of cord blood IgA and allergen-specific IgE and comparison with parental IgE levels and levels at 6 months of age. Results: Forty-six percent of cord blood samples with increased IgE levels (≥0.5 IU/mL) showed indication of maternofetal transfer of IgE. Maternal origin of IgE in these samples was validated by showing reduced levels of IgE at 6 months of age compared with samples with no indication of maternofetal transfer (geometric mean, 9.4 vs 5.4 IU/mL; P = .01). Maternofetal transfer was not appropriately accounted for by the conventional method of cord blood IgA measurement. Conclusions: Maternofetal transfer might be a common cause of increased cord blood IgE levels. Future studies should take potential maternofetal transfer into account or use other markers of atopy. [Copyright &y& Elsevier]

Objective: Cell trafficking during pregnancy results in persistence of small populations of fetal cells in the mother, known as fetal microchimerism (FMc). Changes in cell-free fetal DNA during gestation have been well described, however, less is known about dynamic changes in fetal immune cells in maternal blood. We have investigated FMc in maternal peripheral blood mononuclear cells (PBMC) longitudinally across gestation.Study Design: Thirty-five women with normal pregnancies were studied. FMc was identified in PBMC, CD4+ and CD8+ subsets employing quantitative PCR assays targeting fetal-specific genetic polymorphisms. FMc quantities were reported as fetal genome equivalents (gEq) per 1,000,000 gEq mother's cells. Poisson regression modeled the rate of FMc detection.Main Outcome Measure: FMc in PBMC.Results: The probability of detecting one fetal cell equivalent increased 6.2-fold each trimester [Incidence Rate Ratio (IRR) 95% CI: 1.73, 21.91; p = 0.005]. Although FMc in PBMC was not detected for the majority of time points, 7 of 35 women had detectable FMc during pregnancy at one or more time points, with the majority of positive samples being from the third trimester. There was a suggestion of greater HLA-sharing in families where women had FMc in PBMC. FMc was detected in 9% of CD4+ (2/23) and 18% of CD8+ (3/25) subsets.Conclusions: FMc in PBMC increased as gestation progressed and was found within CD4+ and CD8+ subsets in some women in the latter half of gestation. A number of factors could influence cellular FMc levels including sub-clinical fetal-maternal interface changes and events related to parturition. Whether FMc during pregnancy predicts persistent FMc and/or correlates with fetal-maternal HLA relationships also merits further study. [ABSTRACT FROM AUTHOR]

Abstract: The role of maternal immune cells in early implantation sites has received special attention from reproductive biologists because immune cells participate in tissue transplant rejection. During normal pregnancy, endometrial immune cells differ from those in blood by subset distribution and appear to be activated but non-destructive of conceptuses. The immune system evolved well before placental mammals. By comparing the regulation and functions of endometrial immune cells between species in two phylogenetic clades that model differently evolved placental types (pig (Sus scrofa) versus mouse (Mus musculus) and human (Homo sapiens)), we seek to understand how “non-self” trophoblast cells thrive in most pregnancies. Our studies suggest recruitment of specific immune cells to conceptus-associated endometrium and immune cell-promoted endometrial angiogenesis are of key importance for mammalian conceptus well-being. [Copyright &y& Elsevier]

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Examines cellular immune response, cell proliferation, and messenger ribonucleic acid cytokine expression in fetal pulmonary tissue in the presence or absence of chorioamnionitis. Association between chorioamnionitis and intrauterine inflammatory response of the fetal lung; Inflammatory response of fetal lung tissue with and without exposure to chorioamnionitis; Use of immunohistochemical staining.

Objectives: Altered cytokine expression at the fetoplacental interface may be a potential mechanism for the development of fetal immune dysfunction in children with fetal alcohol syndrome. This study was conducted to determine whether first-trimester trophoblasts respond to ethanol exposure by the induction of specific cytokines.Study Design: HTR-8/SVneo trophoblast cells were cultured in vitro in the presence of either ethanol (0.5% [vol/vol]), lipopolysaccharide (1 microg/mL), or ethanol and lipopolysaccharide. Expression of granulocyte colony-stimulating factor, regulated on activation normal T cell expressed and secreted, and interleukin-6 was examined by Northern analysis and enzyme-linked immunosorbent assay.Results: Culture in the presence of ethanol, lipopolysaccharide, or lipopolysaccharide and ethanol resulted in the increased transcription and secretion of granulocyte colony-stimulating factor, regulated on activation normal T cell expressed and secreted, and interleukin-6 at significantly greater levels (P < .01) than control cultures.Conclusions: Human first-trimester trophoblasts express high levels of cytokines when cultured in the presence of ethanol. Trophoblasts may therefore be an important exogenous source of cytokines for the fetus, and altered cytokine levels during early gestation may have an adverse effect on the development of the fetal immune system. [ABSTRACT FROM AUTHOR]

Determines whether activation of the monocyte-neutrophil system occurs in fetuses before premature birth. Patient characteristics; Clinical and laboratory results; Neonatal outcomes; Activation marker results.

We report a pregnancy complicated by anti-B isoimmunization that resulted in fetal ascites, anemia, hepatomegaly, and polyhydramnios. A previous pregnancy in the same patient was complicated by neonatal ABO incompatibility. A review of the obstetric literature suggests that ABO incompatibility may cause severe fetal anemia, especially in patients with type O blood or a previous history of ABO incompatibility of the newborn. [ABSTRACT FROM AUTHOR]

Abstract: Workshops are an important part of the IFPA annual meeting as they allow for discussion of specialised topics. At IFPA meeting 2011 there were twelve themed workshops, five of which are summarized in this report. These workshops related to various aspects of placental biology: 1) immunology; 2) epigenetics; 3) comparative placentation; 4) trophoblast differentiation; 5) stem cells. [Copyright &y& Elsevier]

Objective: The investigators tested the hypothesis that maternal-fetal immune interactions could be important in initiating spontaneous labor onset by examining if labor was delayed when fetuses share maternal HLA antigen types. Study Design: HLA antigen types A, B, and DR in 200 Danish mother-infant pairs delivering in 42–44 weeks (postterm) were compared with 195 mother-infant pairs delivering in 37–40 weeks (term). Results: Sharing of HLA A and B antigens was more common than expected in postterm deliveries. Odds ratios were 1.54 (95% confidence interval [CI], 1.01–2.35) and 1.75 (95% CI, 0.87–3.52), respectively (risk per shared antigen: 1.40 [95% CI, 1.04–1.90] per unit increase). Adding stringent birth-length criteria for postmaturity (92 cases; 168 controls) strengthened risks associated with antigen sharing to 1.57 (95% CI, 0.90–2.74) and 2.60 (95% CI, 1.15–5.88), respectively (risk per shared antigen: 1.60 (95% CI, 1.10–2.32). Conclusion: Postterm-delivered infants had more HLA A and B antigens in common with their mothers, suggesting that recognition of HLA antigen differences by adaptive immunity may have a role in triggering labor onset. [Copyright &y& Elsevier]

Objective: Progesterone supplementation has been shown to be efficacious in preventing preterm birth. We sought to investigate the effects of progesterone on fetal inflammatory responses. Study Design: Fetal mononuclear cells were isolated from umbilical cord blood and exposed to vehicle or progesterone (P4) for 1 hour prior to lipopolysaccharide (LPS) stimulation. Supernatants were assayed for tumor necrosis factor-α. Similar experiments were performed using cyclic adenosine monophosphate (cAMP) and progesterone modulators. The effect of P4 treatment on intracellular cAMP levels was also determined. Results: LPS treatment led to a significant increase in cytokine production by fetal mononuclear cells. Despite the lack of detectable nuclear progesterone receptors, P4 suppressed this inflammatory response. R5020 (progesterone agonist), forskolin (cAMP inducer), and dibutyryl cAMP (cAMP agonist) all achieved immunosuppression. The cAMP antagonist, Rp-cAMP, blocked the inhibitory effect of progesterone. P4 significantly increased intracellular cAMP levels. Conclusion: Progesterone rapidly suppresses the fetal inflammatory response, possibly via nongenomic activation of the cAMP cascade. [Copyright &y& Elsevier]

Discusses the abstract for the article "The use of mobilized peripheral blood as a donor cell source does not improve chimerism after in utero hematopoietic stem cell transplantation in non-human primates" by Laurence Shields et al published in the December 2003 issue of "American Journal of Obstetrics and Gynecology".

Discusses the abstract for the article "Seroprevalence of bordetella pertussis antibodies in mothers and their newborn infants" by Bernard Gonik et al published in the December 2003 issue of the "American Journal of Obstetrics and Gynecology". Conclusion that a large number of gravidas have low or undetectable pertussis-related antibody levels.

Discusses the abstract for the article "In utero transplantation of autologous and allogeneic fetal liver stem cells in fetal sheep" by Daniel Surbek et al published in the December 2003 issue of the "American Journal of Obstetrics and Gynecology". Conclusion that there are no differences between homing and engraftment capacity of autologous and allogeneic stem cells.

Discusses the abstract for the article "Skin: an active component of the fetal innate immune system" by Yeon Mee Kim et al published in the December 2003 issue of the "American Journal of Obstetrics and Gynecology". Conclusion that fetal skin expresses toll-like receptors in the midtrimester of pregnancy and that the expression of toll-like receptor-2 is increased in chorioamnionitis.

Presents an abstract of `Two Thirds of Human Fetuses with Microbial Invasion of the Aminiotic Cavity Have a Detectable Systemic Cytokine Response Before Birth,' by R. Gomez, F. Ghezzi, et al presented at the 17th Annual Meeting of the Society of Perinatal Obstetricians on January 20-25, 1997 in Anaheim, California.

Presents an abstract of `Combined Prenatal Diagnosis of the RHc, RHE and RHe Fetal Genotype by Polymerase Chain Reaction on Aminiotic Fluid DNA,' by I. Van den Veyver, C. Polon, et al presented at the 17th Annual Meeting of the Society of Perinatal Obstetricians on January 20-25, 1997 in Anaheim, California.

Presents an abstract of `Development of an Allele-Specific Polymerase Chain Reaction Assay for Prenatal Genotyping of the RhC/c and RhE/e Antigen Systems,' by M.J. Hessner, B.S., Atkinson, et al presented at the 17th Annual Meeting of the Society of Perinatal Obstetricians on January 20-25, 1997 in Anaheim, California. Identification of pregnancies at risk for hemolytic disease of the newborn.

Presents an abstract of `The Onset of Spontaneous Preterm Parturition Is Preceded By an Intense Pro-Inflammatory Cytokine Response in the Human Fetus,' by R. Romero, R. Gomez, et al presented at the 17th Annual Meeting of the Society of Perinatal Obstetricians on January 20-25, 1997 in Anaheim, California.

Presents an abstract of the article entitled `Fetal Leukocyte Count: The Effect of Transfusion For Fetal Hemolytic Disease,' by J. Yankowitz et al.

Presents an abstract of the article entitled `Molecular Determination of Fetal Platelet Antigen Status Using Uncultured Amniocytes,' by A. Khouzami et al.

Presents an abstract of the article entitled `Prediction of Fetal Anemia in Red Blood Cell Isoimmunization Not Receiving in Utero Transfusion Using Serial Maternal Antibody Titers,' by S.N. MacGregor et al.

Presents an abstract of the article entitled `Preterm Parturition Is Characterized by In Utero Activation of the Fetal Immune System,' by S. Berry et al.