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Induction of maternal-fetal immune tolerance is essential for the development of normal pregnancy. Impaired expression of costimulatory molecules may lead to intense inflammatory reaction, a mechanism involved in the pathophysiology of gestational diabetes mellitus (GDM). The aim of this study was to investigate whether immunoregulatory molecules are involved in the physiopathology of GDM. This case-control study included 30 healthy pregnant women and 20 GDM patients. Flow cytometry was used to assess peripheral blood T subpopulations (CD4(+) and CD8(+)), the expression of immunoregulatory molecules (CD28, ICOS, CTLA-4, and PD-1) and activation markers (CD69 and HLA-DR). Compared to healthy women, GDM patients had a significantly higher frequency of CD4(+)CD69(+) and CD8(+)CD69(+) T cells; only patients with insulin-treated GDM had increased numbers of CD4(+)HLA-DR(+) T cells. We also observed significantly higher percentages of CD4(+)CD28(+)HLA-DR(+), CD3(+)CD4(+)ICOS(+), CD3(+)CD4(+)PD-1(+), CD8(+)CD28(+)CD69(+), CD8(+)CD28(+)HLA-DR(+), CD8(+)CTLA-4(+)HLA-DR(+), and CD3(+)CD8(+)ICOS(+) T cells and lower frequency of CD3(+)CD4(+)CTLA-4(+), CD3(+)CD8(+)CTLA-4(+), and CD8(+)ICOS(+)HLA-DR(+) T cells in GDM patients compared to healthy pregnant women. This first study assessing costimulatory molecules in GDM patients shows that these patients have exacerbated markers of T cell activation along with CTLA-4 deficiency, findings that indicate that the maternal-fetal tolerance is compromised in these patients.

Objective To assess correlations between maternal serum levels of pro- and anti-angiogenic factors with uterine perfusion in women with early- compared with late-onset preeclampsia, and in healthy pregnant women. Design Case-control study. Setting Antenatal care clinic located within a hospital (Sao Bernardo do Campo, Brazil). Population We enrolled 54 preeclamptic and 54 healthy control women who were coming for routine ultrasound at 28–36 weeks' gestation. Methods All participants had uterine artery and umbilical Doppler studies and a blood sample to assess maternal serum levels of soluble fms-like tyrosine kinase-1, soluble endoglin, adiponectin and plasminogen activator inhibitor-1. All angiogenic factors were measured using enzyme-linked immunosorbent assay. Main outcome measures Levels of pro- and anti-angiogenic factors in maternal serum, and uterine artery Doppler findings. Results Concentrations of soluble fms-like tyrosine kinase-1 and soluble endoglin were significantly higher in preeclamptic than control women (p

The relevance of gene polymorphisms in the development of unexplained recurrent spontaneous abortion is still unclear. Cytokines, angiogenic mediators, and hormones are involved in all stages of reproduction and pregnancy outcome. Impaired production and/or unbalanced ratios of these mediators have been implicated in the pathogenesis of unexplained recurrent spontaneous abortion. Functional polymorphism influence gene activity and therefore can interfere with the expression of mediators. Several studies have been carried out to evaluate the relationship between cytokines, angiogenic mediators, and hormones gene polymorphisms and unexplained recurrent spontaneous abortion. The results of these studies are mostly contradictory, and few significant associations have been identified. Up to present time, the evidence is insufficient to support the evaluation of cytokines, angiogenic mediators, and hormones gene polymorphism in routine workup in all cases of recurrent pregnancy loss, and these tests are not included in any of the major obstetric guidelines.

Galectins are proteins with the ability to bind β-galactosides through a conserved carbohydrate recognition domain. Galectin-1 exerts its biological effects by binding glycan ligands on proteins involved in cell adhesion and growth regulation. Galectin-1 inhibits trophoblast cell proliferation and induces syncytium formation. Its down-regulation in the syncytiotrophoblast has been associated with early pregnancy loss. In the choriocarcinoma-derived BeWo cells the galectin-1 induced growth inhibition is apoptosis-independent, but rather appears to be mediated by binding to cell surface receptors, such as the receptor tyrosine kinases REarranged during Transfection (RET) and Janus Kinase (JAK) 2 as well as vascular endothelial growth factor receptor 3. On the syncytiotrophoblast and extravillous trophoblast galectin-1 binds the Thomsen–Friedenreich disaccharide on mucin-1. The cell differentiation processes induced by binding to these receptors ultimately lead to the inhibition of proliferation and syncytium formation.

The incidence of gestational diabetes (GD) is rising worldwide, in parallel with obesity and type 2 diabetes. Obesity and GD are conditions that have in common a state of chronic, low-grade subclinical inflammation characterized by abnormal production of cytokines and mediators. Genetic polymorphisms may influence the production of inflammatory mediators and predispose to different disorders, including diabetes. The aim of this study was to review the existing literature on the relationship between inflammatory mediator gene polymorphisms and GD. The search in PubMed was restricted to articles published in English, from January 1990 to December 2010. Eight studies were included. These publications evaluated 13 different SNPs and six inflammatory mediators in the blood of women with GD. Gene polymorphisms related to leptin, mannose-binding lectin (MBL) and RAGE (receptor for advanced glycation end products) were individually evaluated in a single study each. Leptin and MBL plasma levels were also evaluated in two studies. The participants included in the studies were ethnically different, but matched with controls. Different criteria were adopted to select the participants. Seven of the eight studies included took into consideration the BMI of patients and controls. Due to the heterogeneity and limited number of studies on GD and inflammatory gene polymorphisms, we could not pool together any of the results or perform any additional analyses of the existing data. Since the existing findings come from isolated studies with mostly small sample sizes, there is a need for new, larger, properly designed studies of good methodological quality.

Citation Junovich G, Mayer Y, Azpiroz A, Daher S, Iglesias A, Zylverstein C, Gentile T, Pasqualini S, Markert UR, Gutierrez G. Ovarian stimulation affects the levels of regulatory endometrial NK cells and angiogenic cytokine VEGF. Am J Reprod Immunol 2011; 65: 146–153 Problem Endometrial NK cells play a critical role in uterine vascularization producing angiogenic factors. Impact of ovarian stimulation on endometrial expression of NK cells and VEGF in normal fertile oocyte donors and the effect of endometrial injury treatment on these parameters have been investigated. Method of study Endometrial tissue was obtained from oocyte donors during natural and stimulated cycles. NK cell subsets were measured by flow cytometry. VEGF was determined by ELISA and flow cytometry. Endometrial angiogenic parameters were determined by ultrasound Doppler. Local injury was induced by scratching endometrial tissue previous to implantation window. Results Ovarian stimulation decreased endometrial levels of NK cells and vascularization index but increased VEGF levels. Local injury normalized only the CD56+ NK cell count. Conclusion Hormonal therapy for ovarian stimulation may be associated with poor endometrial vascularization. Local injury before the implantation window seems not to influence endometrial angiogenic parameters altered by ovarian stimulation.

The clinical spectrum of preeclampsia (PE) ranges from mild hypertension to severe vasospasm associated with convulsions and multiple organ damage. The biological factors that determine the progression of PE to eclampsia (E) are unknown. Endothelial cell activation seems related to an impaired maternal immune response. The production of cytokines, IL-10 and TGF-beta1, is apparently suppressed, and altered IL-2/IL-10 and TNF-alpha/IL-10 ratios have been reported in preeclamptic cases. The relationship between PE and cytokine gene polymorphism has been studied, but there are few studies that include eclamptic patients. This study aimed at investigating whether polymorphisms in genes, TNF-alpha promoter (-308 GA), IL6 promoter (-174 GC), IFN-gamma intron 1 (+874 AT), IL10 promoters (-1082 AG), (-819 CT) and (-592 CA) and TGF-beta1 codon 10 (+869 TC) and codon 25 (+915 GC) are associated with E and/or PE. Genotyping was carried out in 266 Mulatto women from the northeastern region of Brazil who were referred to a single maternity hospital: 92 with PE, 73 with E and 101 normotensive controls. The chi(2) or Fisher's exact tests were used to compare genotype frequencies. Among the six single-nucleotide polymorphisms (SNPs) studied, we found no difference in genotype frequencies between the groups. There was a higher frequency of IFN-gamma (+874 A) in eclamptic patients in comparison with that in controls. (70.3 vs. 57.8%, respectively; P=0.02). There were no other significant differences in allelic frequencies between eclamptic, preeclamptic and control groups We found no independent association between any single SNP and PE or E risk in this population of Mulatto women from the northeastern region of Brazil.

Aim: Considering the roles of c-erB-2 and p53 oncoproteins in tumor progression, we aimed to evaluate their expression in hydatidiform moles, and the possible predictive value of this immunoexpression in postmolar follow-up. Methods: Group I comprised 35 patients with progression to gestational trophoblastic tumor, and group II included 32 patients with progression to spontaneous remission. Immunohistochemical tests were performed by streptavidin-peroxidase method. c-erbB-2 immunoexpression was evaluated according to quantitative and semiquantitative criteria; p53 according to percentage of cells with stained nuclei. Data were analyzed by Student t-test, Mann–Whitney test, ROC curve and logistic regression analysis. Results: c-erbB-2 and p-53 expressions were significantly increased in group I. Quantitative and semiquantitative analysis of c-erb-2 showed that its expression may be associated with mole hydatidiform progression to gestational trophoblastic tumor. Taking into account cells with complete membranous delineation we proposed a cut-off value of 10.8%. Similarly, considering the percentage of cells presenting nuclei marked by p53 we suggested a cut-off value of 40.1% for the prediction of malignant transformation of mole hydatidiform. Conclusions: c-erbB-2 and p53 immunoexpression in hydatidiform mole are usually increased with malignant transformation. In addition to β-fraction of human chorionic gonadotropin, they could possibly help the establishment of a therapeutic protocol.

Problem Considering that cytokines are involved in preeclampsia (PE) pathogenesis and that cytokine gene polymorphism may affect cytokine production, our purpose was to investigate the association of PE with tumor necrosis factor (TNF)-α (−308), transforming growth factor-β1 (+10; 25), interleukin (IL)-10 (−1082), IL-6 (−174), and interferon-γ (+874) polymorphisms. Method of study Genotyping was performed in women with PE (56 White and 95 non-White women) and in women without obstetric pathology (92 White and 97 non-White women). Data were analyzed by the chi-square or Fisher exact test. We performed a meta-analysis encompassing these and results from other laboratories on the association of TNF-α polymorphisms and PE. Results We observed a lower frequency of the IL-10 −1082-G/G genotype in White women with PE (PE: 5%; Control (C): 15%, P = 0.02) and no association for all other polymorphisms, including meta-analysis of TNF-α results. Conclusion Our study suggests that PE is associated with IL-10-(1082) polymorphism but not with TNF-(308) polymorphism. On the basis of meta-analysis, we confirm the need for more studies for the evaluation of cytokine genotype in disease.

BACKGROUND: In view of evidence suggesting an immunological cause of recurrent spontaneous abortions (RSA) and the large number of maternal natural killer (NK) cells present in the pregnant uterus, we investigated the genetic polymorphism of the killer cell immunoglobulin-like receptors (KIR) in women with RSA. METHODS: KIR gene repertoire and KIR2DL4 (a receptor for HLA-G) genotyping were determined by SSP and SSCP respectively, in women experiencing RSA and controls. RESULTS: The KIR repertoire did not differ between RSA patients and controls in terms of: (i) the number of inhibitory receptors; (ii) the number of activating receptors; (iii) the ratio of inhibitory to activating receptors. KIR2DL4, a receptor for HLA-G, has different transmembrane alleles, which produce functionally different phenotypes. The frequency of KIR2DL4 transmembrane genotypes differed significantly between RSA patients and controls (P = 0.03). However, although homozygosity for a membrane-bound receptor was more frequent in patients (25%) than controls (10%), other genotypes that would produce the same phenotype were not more frequent in patients than controls. CONCLUSIONS: The data provide little evidence that KIR polymorphism plays a role in predisposition to RSA.

Cytokines seem to play a critical role in the pathogenesis of unexplained recurrent pregnancy loss (RPL). Th1 cytokines have been shown to exert deleterious effects on pregnancy, inhibiting foetal growth and development. On the other hand, Th2 cytokines have been associated with successful pregnancy. The purpose of this study was to evaluate cytokine production in women with RPL. The studied group comprised 29 women with RPL, with at least three consecutive spontaneous abortions. The control group included 27 women with a history of successful pregnancies and no miscarriage. We determined IL-6 and TNF-alpha production in peripheral blood cultured with LPS, as well as IFN-gamma and TGF-beta induced by PHA stimulation. Cytokines were measured by enzyme-linked immunoabsorbant assay (ELISA) using commercial kits (RD, Amersham-Pharmacia). Mann-Whitney test was applied to compare differences between groups. The level of significance was defined at P < 0.05. We observed significantly higher levels of IFN-gamma (355.8 pg/ml versus 98.0 pg/ml; P = 0.01) and a trend toward increased TNF-alpha production (2410.2 pg/ml versus1980.2 pg/ml; P = 0.07) in RPL women as compared to controls. In relation to IL-6 and TGF-beta, no significant difference was detected between RPL and control groups. In agreement with experimental observations, our data support the hypothesis of Th1 cytokine involvement in the pathogenesis of RPL.

Since certain cytokines may play a role in unexplained recurrent pregnancy loss (RPL) and also some cytokine gene polymorphisms may affect the level of cytokine production, the aim of the present study was to investigate the relationship between RPL and polymorphisms of the genes coding for TNF-alpha (-308 G--A), IL-10 (-1082 G--A), IL-6 (-174 G--C), and IFN-gamma (+874 A--T). Genotyping was performed in 48 RPL women and 108 ethnically matched healthy individuals. In addition, we performed a meta-analysis encompassing the present results and those from studies on the association of TNF-alpha, IL-10 and IFN-gamma polymorphisms with RPL published in the literature until December 2001. The results showed: (1) no evidence of association with IL-6 gene polymorphisms; (2) significant associations, revealed by the meta-analysis, with the high cytokine production genotypes of IFN-gamma (+874 T/T: odds ratio (OR)=1.92, P=0.04) and IL-10 (-1082 G/G: OR=1.75, P=0.03), and a trend for association with the high TNF-alpha production genotypes -308 A/A and A/G (OR=1.61; P=0.18). We believe that the associations of these genotypes with RPL are interesting not only as risk factors but also because they represent another piece of evidence that these cytokines might be important in the pathogenesis of RPL.

Cow's milk protein (CMP) allergy was investigated in 25 children (age-range 3 months to 11 years) with chronic constipation. A diagnosis of constipation was made on the basis of a history of painful elimination of hard stools for at least 1 month, whether or not associated with a reduced frequency of stools or soiling. The children were evaluated using clinical parameters and the following laboratory tests: total serum immunoglobulin E (IgE); specific IgE (radioallergosorbent test [RAST]) for whole cow's milk, alpha-lactoalbumin, beta-lactoglobulin, and a food group; and skin-prick tests with whole milk, alpha-lactoalbumin, beta-lactoglobulin, and casein. Following the evaluation, the children were submitted to a CMP-free diet for a period of 4 weeks. In seven patients (28%), constipation disappeared during the CMP-free diet and reappeared within 48-72 h following challenge with cow's milk. In two infants a rectal biopsy revealed allergic colitis and they therefore did not undergo the challenge. High serum levels of total IgE were observed in five of the children who showed a clinical improvement (71%), a positive skin-test in two (29%), and detectable specific IgE in two (29%). These results suggest that CMP allergy or intolerance should be considered as a cause of chronic refractory constipation in children, although the underlying mechanism still require further investigation.

Introduction Trophoblast cell invasion is one of key steps for successful pregnancy, which is controlled by several factors including cytokines that activate intracellular signaling cascades including the Janus kinase / signal transducer and activator of transcription (JAK-STAT) system. Objectives We aimed to analyze the effect of cytokines on STAT1 expression and trophoblast cell functions. Methods Immortalized HTR-8/SVneo cells were treated with interleukin-6 (IL-6) IL-11, granulocyte macrophage colony-stimulating factor (GM-CSF), leukemia inhibitory factor (LIF) and oncostatin M (OSM). STAT1 phosphorylation (tyr-701) was analyzed by Western blotting and immunofluorescence staining. Simultaneously, cells were incubated with 50 μ M Fludarabine (specific STAT1 inhibitor) or small interfering RNA (siRNA) to inhibit the expression of STAT1 and followed by cytokine stimulation. STAT1 DNA-binding activity, cell viability and invasion were analyzed by DNA-binding, MTS and Matrigel invasion assays. Results Western blot analysis and immunofluorescence staining of STAT1 phosphorylation revealed that OSM induced phosphorylation of STAT-1 stronger than LIF in HTR-8/SVneo. IL-6, IL-11 and GM-CSF had no effect on STAT1 activation. STAT1 phosphorylation was inhibited by STAT1 siRNA and Fludarabine. STAT1 inhibition reduced STAT1 DNA binding activity and OSM could not rescue this effect. OSM stimulated HTR-8/SVneo cell viability and invasion, whereas STAT1 inhibition decreased trophoblast cell invasion. This reduction could not be prevented by OSM. Conclusions These findings demonstrate that the OSM-STAT1 axis plays an important role in trophoblastic cells and STAT1 activation may induce a variety of cell functions

Placental apoptosis-associated protein imbalance might contribute to the pathogenesis of pre- and post-term birth. Therefore, we evaluated the expression and distribution of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) molecules in term, pre-term and post-term placentas.Placental samples were collected from women with term (n = 25), pre-term (n = 7) and post-term (n = 10) deliveries. The expression of Bcl-2 and Bax was assessed by immunochemistry on paraffin-embedded placental specimens.The pattern of immunostaining for Bcl-2 and Bax was the same in all samples, but not the intensity. The Bax/Bcl-2 ratio was higher in both pre-term and post-term placental samples compared with term placentas as a result of intense reactivity for the pro-apoptotic factor, Bax in pre-term and post-term placentas and, for Bcl-2 decrease in pre-term placentas.These findings suggest that different unbalance mechanisms in placental apoptotic-associated protein expressions may be involved in the physiopathology of pre-term and post-term births.

s / Placenta 36 (2015) 469e521 519 PB.43. VITAMIN D AND GESTATIONAL DIABETES MELLITUS: PHENOTYPE AND GENOTYPE ANALYSIS K.P.T. Pendeloski, T.F. Lobo, C.M.Y. Ohki, T.W. Siqueira, J.F. Fantasia, M.R. Torloni, R. Mattar, S. Daher. Department of Obstetrics, Universidade Federal de S~ ao Paulo, Sao Paulo, Brazil Objectives: Patients with Gestational Diabetes Mellitus (GDM) have an inflammatory process and insulin resistance which are more intense than women having a physiological pregnancy. Vitamin D plays a role in the control of both inflammation and insulin resistance. Polymorphism in the vitamin D VDR Fok-I gene may affect the expression of this molecule. We evaluated the levels of soluble vitamin D and vitamin D VDR (Fok-I rs10735810) gene polymorphism in GDM patients and healthy controls. Methods: This case-control study included 108 participants in the third trimester of pregnancy: 58 healthy women (control group) and 50 with GDM. Vitamin D serum levels were determined by HPLC. Polymorphism genotyping was obtained by PCR-RFLP. Data were analyzed by Student t and Chi-square tests and significance was set at p < 0.05. Results: There were no significant differences in vitamin D serum levels between the groups (Control x GDM: 19.95 ± 9.35 ng/mL 23.93 ± 12.21 ng/mL, respectively, p 1⁄4 0.09). Genotypic frequencies of VDR Fok-I were 62% FF, 34% Ff and 4% ff in controls, and 50% FF, 36% Ff and 14% ff in the GDM group (p 1⁄4 0.17). There was no association between GDM and the polymorphism analyzed, or between vitamin D genotype/phenotype. Conclusion: GDM was not associated with differences in vitamin D serum levels or with Fok-I VDR polymorphism. Financial support: CNPq (307337/2012-0). PB.44. DOES IN UTERO EXPOSURE TO HUMAN CHORIONIC GONADOTROPIN (HCG) HAVE A PROTECTIVE EFFECT ON HORMONAL IMBALANCES IN TRANSGENIC MICE? Laura D. Ratner , Guillermina Stevens , Carla Marcial , Paula Farre , Matti Poutanen , Ricardo Calandra , Ilpo Huhtaniemi , Susana B. Rulli . 1 Institute of Biology and Experimental Medicine (IBYME-CONICET), Buenos Aires, Argentina; Department of Physiology, University of Turku, Finland; 3 Imperial College London, London, United Kingdom We have previously developed a transgenic mouse model for the human chorionic gonadotropin b-subunit (hCGb+), which exhibits constitutively elevated levels of hCG and increased production of testosterone, progesterone and prolactin from early age. The adult females are infertile, obese, and insulin-resistant and develop pituitary and mammary tumors. After normalization of the prolactin levels by treatment with the dopamine agonist cabergoline, these females become fertile. Objective: To analyze the influence of hCG exposure in utero on the reproductive and metabolic function of the female offspring at adulthood. Methods: hCGb+ females pre-treated with cabergoline (500 mg/dose for one week) at 5 weeks of age were crossbred with wild-type FVB/n males (WT). Female offspring were analyzed for reproductive and metabolic functions at adulthood. Results: the offspring were exposed to the effects of elevated levels of maternal hCG during gestation (WT: 1.8 ± 0.1, hCGb+: 23.4 ± 8.5 mIU/ml, p < 0.01), but with normal values of steroids and prolactin. Eighty percent of the transgenic female offspring exhibited normalized pituitary and body weights as well as normal estrous cycles and gonadal function. These mice were fertile, and gave birth to several litters with similar results. The metabolic disturbances, in terms of glucose and insulin tolerance test (p < 0.01), and basal triglyceride levels were also normalized (p < 0.01). Conclusions: We found that hCG hypersecretion during pregnancy had a significant impact on the transgenic offspring’s phenotype. These results suggest that the presence of hCG during gestation may have a protective effect on the transgenic offspring, by preventing them from hormone imbalances, which led to infertility and metabolic disturbances at adulthood. This is the first mouse model in which gestation occurs in the presence of hCG, and paves the way for future investigations related to extragonadal functions of hGC. Further studies are necessary to understand the mechanism involved in this phenomenon. PB.45. IN VIVO ANALYSIS OF OXIDATIVE STRESS RELATIONSHIP IN EMBRYOFETAL PANCREAS DEVELOPMENT OF THE OFFSPRING OF DIABETIC RATS I.L. Iessi , Y.K. Sinzato , F.Q. Gallego , B. Dallaqua , R.L. Amorim , C.E.F. Alves , I.M.P. Calderon , M.V.C. Rudge , D.C. Damasceno . 1 Laboratory of Experimental Research on Gynecology and Obstetrics, Graduate Program on Gynecology, Obstetrics and Mastology, Botucatu Medical School, Brazil; Department of Pathology, Botucatu Veterinary and Zootechnology School, Univ. Estadual Paulista e UNESP, Botucatu, S~ ao Paulo, Brazil Background: Rat offspring exposed to a hyperglycemic intrauterine environment present alterations in pancreatic hormone levels at birth. Our hypothesis is that the association of maternal hyperglycemia and exacerbated oxidative stress status are involved in the embryofetal pancreatic development impairment. Aim: To evaluate the oxidative stress status in embryofetal pancreatic development in hyperglycemic conditions. Methods: The rats were randomly assigned into: Non diabetic (Control 1⁄4 C, glycemia < 120 mg/dL), Mild diabetes (MD e Streptozotocin, 100 mg/kg b.w., sc.) and Severe diabetes (SD e STZ, 40 mg/kg b.w., i.v.). After mating, on days 11.5, 18.5 and 21 of pregnancy, the dams were killed to obtain their embryo/fetal pancreas for antioxidant enzymes expression and for morphological and immunohistochemistry analyses. p < 0.05 was considered as a significant statistical limit. Results: The expression of antioxidant enzymes showed no difference in the embryonic period and the islet number, islet area and the minor diameter also showed no alterations at fetal period in all groups. However, the major diameter was increased in islets of SD fetuses on day 21 of pregnancy in relation to the others. Insulin immunolocalization in the SD and MD groups was decreased as compared to the C group on day 18.5 and the SD group also presented reduction at term in relation to the others. Glucagon immunolocalization was decreased in SD fetuses on day 18.5 of pregnancy in relation to the C group. There was a reduction of in caspase-3 in the SD group on day 18.5 of pregnancy and an increase in the MD group at term compared to the C group. There was no difference in Ki67 compared to the others. Conclusion: The hyperglycemic intrauterine environment caused no alterations in protein expression. However it caused damages in the pancreatic islet morphometry and hormonal immunolocalization in the fetal development, which might contribute to later alterations in adult life. Acknowledgement: FAPESP/Brazil (Process numbers: 2011/18519-7, 2012/ 23642-2). PB.46. INFLUENCE OF TOXOPLASMA GONDII INFECTION IN THE COMMUNICATION BETWEEN HUMAN EXTRAVILLOUS TROPHOBLAST CELLS AND MACROPHAGES P.M. Guirelli , F.C. Oliveira , M.B. Angeloni , B.F. Barbosa , A.O. Gomes , A.S. Castro , P.S. Franco , R.J. Silva , J.R. Mineo , F. Ietta , E.A. Ferro . 1 Laboratory of Histology and Embryology, Institute of Biomedical Sciences, Federal University of Uberlândia, Av. Par a, 1720, 38405-320 Uberlândia, MG, Brazil; 2 Laboratory of Immunoparasitology, Institute of Biomedical Sciences, Federal University of Uberlândia, Av. Par a, 1720, 38405-320 Uberlândia, MG, Brazil; Department of Life Science, University of Siena, Aldo Moro Road 2, Siena, Italy The interaction between human extravillous trophoblast cells and macrophages plays an important role in implantation and placentation during a successful pregnancy. However, any dysfunction in this communication is associated with pregnancy complications. Objectives: The aim of this study was to investigate the influence of Toxoplasma gondii in the occurrence of apoptosis triggered by macrophages in HTR-8/SVneo cells.

The purpose of the present study was to analyze the frequency of HLA-DR and DQ antigens in Brazilian asthmatic children with skin-test and RAST positivity to Dermatophagoides pteronyssinus. The comparison of HLA-DR and DQ antigenic frequencies between patients (n = 30) and controls disclosed a significantly higher HLA-DQ2 frequency in the patients (60% versus 34%, p = 0.013; R. R. = 2.8).

The 29th Annual Meeting of the American Society for Reproductive Immunology was held on 5–9 June 2009, in Orlando (FL, USA). Peter Hansen and Mary Brown co-chaired the conference. The co-chairs and a scientific committee put together an outstanding program that included the most contemporary topics in reproductive immunology, with special focus on intrauterine infections and reproductive anomalies. A highlight of the meeting was the pre-meeting postgraduate course, which was attended by a large group of young investigators and trainees. The participants in the postgraduate course and the main meeting represented an international milieu of investigators, students and health professionals.