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Maternal Immune Response (maternal + immune_response)
Selected AbstractsREVIEW ARTICLE: Maternal Immune Responses to Trophoblast: The Contribution of the Horse to Pregnancy ImmunologyAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2010Leela E. Noronha Citation Noronha LE, Antczak DF. Maternal immune responses to trophoblast: the contribution of the horse to pregnancy immunology. Am J Reprod Immunol 2010 The horse has proven to be a distinctively informative species in the study of pregnancy immunology for several reasons. First, unique aspects of the anatomy and physiology of the equine conceptus facilitate approaches that are not possible in other model organisms, such as non-surgical recovery of early stage embryos and conceptuses and isolation of pure trophoblast cell populations. Second, pregnant mares make strong cytotoxic antibody responses to paternal major histocompatibility complex class I antigens expressed by the chorionic girdle cells, permitting detailed evaluation of the antigenicity of these invasive trophoblasts and how they affect the maternal immune system. Third, there is abundant evidence for local maternal cellular immune responses to the invading trophoblasts in the pregnant mare. The survival of the equine fetus in the face of strong maternal immune responses highlights the complex immunoregulatory mechanisms that result in materno,fetal tolerance. Finally, the parallels between human and horse trophoblast cell types, their gene expression, and function make the study of equine pregnancy highly relevant to human health. Here, we review the most pertinent aspects of equine reproductive immunology and how studies of the pregnant mare have contributed to our understanding of maternal acceptance of the allogeneic fetus. [source] ORIGINAL ARTICLE: HLA-G Expression Is Up-Regulated by Progesterone in Mesenchymal Stem CellsAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 1 2009Ekaterina Ivanova-Todorova Problem, Maternal immune response to fetal tissues is modified in such way that it favors the development of pregnancy. Human leukocyte antigen (HLA)-G, progesterone and mesenchymal stem cells (MSCs) have been identified as potent immunomodulatory agents in different experimental systems and the interactions between these three factors are studies in this paper. Method of study, Human MSCs are isolated from human adipose tissue, bone marrow and decidua are cultured in the presence of progesterone and the expression of HLA-G is followed-up at protein and mRNA levels. Results, The MSCs cultured in the presence of progesterone express increased levels of both cell surface and cytoplasmic HLA-G when compared with the control MSCs. Conclusion, Progesterone up-regulates the expression by MSCs of HLA-G which is a major player in maintenance of the immune balance between the mother and the fetus. MSCs are newly detected targets of progesterone with well documented immunomodulatory activity. [source] REVIEW ARTICLE: Maternal Immune Responses to Trophoblast: The Contribution of the Horse to Pregnancy ImmunologyAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2010Leela E. Noronha Citation Noronha LE, Antczak DF. Maternal immune responses to trophoblast: the contribution of the horse to pregnancy immunology. Am J Reprod Immunol 2010 The horse has proven to be a distinctively informative species in the study of pregnancy immunology for several reasons. First, unique aspects of the anatomy and physiology of the equine conceptus facilitate approaches that are not possible in other model organisms, such as non-surgical recovery of early stage embryos and conceptuses and isolation of pure trophoblast cell populations. Second, pregnant mares make strong cytotoxic antibody responses to paternal major histocompatibility complex class I antigens expressed by the chorionic girdle cells, permitting detailed evaluation of the antigenicity of these invasive trophoblasts and how they affect the maternal immune system. Third, there is abundant evidence for local maternal cellular immune responses to the invading trophoblasts in the pregnant mare. The survival of the equine fetus in the face of strong maternal immune responses highlights the complex immunoregulatory mechanisms that result in materno,fetal tolerance. Finally, the parallels between human and horse trophoblast cell types, their gene expression, and function make the study of equine pregnancy highly relevant to human health. Here, we review the most pertinent aspects of equine reproductive immunology and how studies of the pregnant mare have contributed to our understanding of maternal acceptance of the allogeneic fetus. [source] The mother-offspring dyad and the immune systemACTA PAEDIATRICA, Issue 3 2000LÅ Hanson A. The mother and the fetus. The mother's immune system reacts against the fetus and there is therefore a risk of destruction of or damage to the fetus. We are now beginning to understand some of the mechanisms that protect the fetus, but, when these are defective, intrauterine growth retardation or abortions may ensue. However, the cytokines of this maternal immune response to the fetus also monitor different phases of pregnancy, starting with effects on the ovarium and involving preparation of the decidua for the implantation of the fertilized egg, the growth of the trophoblasts, the production of hormones important for the pregnancy and finally of the prostaglandins that induce delivery. B. The mother and the child. Human milk contains anti-idiotypic antibodies which after transfer to the offspring are capable of enhancing antibody responses. Human milk contains numerous leucocytes especially during early lactation. There is increasing evidence that milk lymphocytes are taken up by the breastfed infant, which seems to have become tolerant to maternal HLA. Breastfeeding mothers are therefore good donors of renal transplants to their breastfed offspring in adult age, too. Conclusion: It is suggested that the milk lymphocytes may be taken up by the offspring and that immunological information is thereby carried over from the mother. This mechanism may explain why breastfeeding seems to confer enhanced protection against infections also some years after the termination of breastfeeding. [source] REVIEW ARTICLE: Placental Apoptosis in Health and DiseaseAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2010Andrew N. Sharp Citation Sharp AN, Heazell AEP, Crocker IP, Mor G. Placental apoptosis in health and disease. Am J Reprod Immunol 2010; 64: 159,169 Apoptosis, programmed cell death, is an essential feature of normal placental development but is exaggerated in association with placental disease. Placental development relies upon effective implantation and invasion of the maternal decidua by the placental trophoblast. In normal pregnancy, trophoblast apoptosis increases with placental growth and advancing gestation. However, apoptosis is notably exaggerated in the pregnancy complications, hydatidiform mole, pre-eclampsia, and intrauterine growth restriction (IUGR). Placental apoptosis may be initiated by a variety of stimuli, including hypoxia and oxidative stress. In common with other cell-types, trophoblast apoptosis follows the extrinsic or intrinsic pathways culminating in the activation of caspases. In contrast, the formation of apoptotic bodies is less clearly identified, but postulated by some to involve the clustering of apoptotic nuclei and liberation of this material into the maternal circulation. In addition to promoting a favorable maternal immune response, the release of this placental-derived material is thought to provoke the endothelial dysfunction of pre-eclampsia. Widespread apoptosis of the syncytiotrophoblast may also impair trophoblast function leading to the reduction in nutrient transport seen in IUGR. A clearer understanding of placental apoptosis and its regulation may provide new insights into placental pathologies, potentially suggesting therapeutic targets. [source] ORIGINAL ARTICLE: Temporal and Spatial Expression of Tumor-Associated Antigen RCAS1 in Pregnant Mouse UterusAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 2 2010Ekaterine Tskitishvili Citation Tskitishvili E, Nakamura H, Kinugasa-Taniguchi Y, Kanagawa T, Kimura T, Tomimatsu T, Shimoya K. Temporal and spatial expression of tumor-associated antigen RCAS1 in pregnant mouse uterus. Am J Reprod Immunol 2010; 63: 137,143 Problem, The tumor-associated antigen RCAS1 (receptor-binding cancer antigen expressed on SiSo cells) is considered to play a role in the inhibition of maternal immune response during pregnancy, and participates in the initiation of labor and placental detachment. The aim of our study was to investigate the expression of RCAS1 protein in the uteri of normal pregnant mice. Method of study, Uteri with fetuses were collected from pregnant ICR mice on days 1.5, 3.5, 5.5, 7.5, and 9.5 p.c., and uterine and placental tissues were obtained separately on days 11.5, 13.5, 15.5, and 17.5 p.c. Samples were examined using real-time (RT)-PCR, Western blotting, and immunohistochemical analyses. Results, In normal pregnant mice, RCAS1 protein mRNA was significantly increased on day 7.5 p.c. Antigen localization was detected in the placenta, decidua, and fetus. Conclusion, The results of this study suggest the importance of day 7.5 p.c. for RCAS1 protein expression in connection with placentation as a possible target for future in vivo studies. [source] ORIGINAL ARTICLE: Impact of Female Sex Hormones on the Maturation and Function of Human Dendritic CellsAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2009Sabine E. Segerer Problem, During pregnancy, the immune and the endocrine system cooperate to ensure that the fetal allograft develops without eliciting a maternal immune response. This is presumably in part achieved by dendritic cells (DCs) that play a dominant role in maintaining peripheral tolerance. In this study, we investigated whether female sex hormones, such as human chorionic gonadotropin (hCG), progesterone (Prog), and estradiol (E2), which are highly elevated during pregnancy, induce the differentiation of DCs into a tolerance-inducing phenotype. Methods/Results, Immature DCs were generated from blood-derived monocytes and differentiated in the presence of hCG, Prog, E2, or Dexamethasone (Dex) as a control. Unlike Dex, female sex hormones did not prevent the upregulation of surface markers characteristic for mature DCs, such as CD40, CD83, and CD86, except for hCG, which inhibited HLA-DR expression. Similarly, hCG, Prog, and E2 had any impact on neither the rearrangement of the F-actin cytoskeleton nor the enhanced chemokine secretion following DC maturation, both of which were strongly altered by Dex. Nevertheless, the T-cell stimulatory capacity of DCs was significantly reduced after hCG and E2 exposure. Conclusion, Our findings suggest that the female sex hormones hCG and E2 inhibit the T-cell stimulatory capacity of DCs, which may help in preventing an allogenic T-cell response against the embryo. [source] REVIEW ARTICLE: Human NK Cells in Pregnant Uterus: Why There?AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 5 2008Philippe Le Bouteiller Human Natural Killer (NK) cells are present in great number in pregnant uterine mucosa. They must be there for specialized functions, but which ones? This review discusses important recent observations that further contribute to this fascinating debate. Firstly, an array of corroborating findings indicates that uterine NK cell proliferation is synchronized with the cyclic surge of progesterone. Secondly, uterine NK cells are unlikely to exert a direct control on the embryo implantation. Thirdly, these NK cells influence the uterine vascular remodeling in early pregnancy but might not be the single key element that control trophoblast invasion. Finally, uterine NK cells are likely to be an important component of the local maternal immune response to pathogen infections. [source] REVIEW ARTICLE: Maternal Immune Responses to Trophoblast: The Contribution of the Horse to Pregnancy ImmunologyAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2010Leela E. Noronha Citation Noronha LE, Antczak DF. Maternal immune responses to trophoblast: the contribution of the horse to pregnancy immunology. Am J Reprod Immunol 2010 The horse has proven to be a distinctively informative species in the study of pregnancy immunology for several reasons. First, unique aspects of the anatomy and physiology of the equine conceptus facilitate approaches that are not possible in other model organisms, such as non-surgical recovery of early stage embryos and conceptuses and isolation of pure trophoblast cell populations. Second, pregnant mares make strong cytotoxic antibody responses to paternal major histocompatibility complex class I antigens expressed by the chorionic girdle cells, permitting detailed evaluation of the antigenicity of these invasive trophoblasts and how they affect the maternal immune system. Third, there is abundant evidence for local maternal cellular immune responses to the invading trophoblasts in the pregnant mare. The survival of the equine fetus in the face of strong maternal immune responses highlights the complex immunoregulatory mechanisms that result in materno,fetal tolerance. Finally, the parallels between human and horse trophoblast cell types, their gene expression, and function make the study of equine pregnancy highly relevant to human health. Here, we review the most pertinent aspects of equine reproductive immunology and how studies of the pregnant mare have contributed to our understanding of maternal acceptance of the allogeneic fetus. [source] ORIGINAL ARTICLE: Syngeneic Immune-Dependent Abortions in Mice Suggest Paternal Alloantigen-Independent MechanismsAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2008Jean A. Kundert Problem, Recurrent immune-associated miscarriages in humans are thought to result from maternal immune responses to paternal alloantigens. We investigated the role of paternal alloantigens in a mouse model of immune-dependent abortion. Method of study, Sib-crosses of C57Bl/6J (haplotype b/b) mice heterozygous for a targeted hypomorphic allele of the tbp gene (tbp,,/+) resulted in selective mid-gestational abortion of 88% of the tbp,,/,, fetuses. In dams lacking mature lymphocytes (rag1,/,), nearly all tbp,,/,, fetuses survived to birth, indicating abortions were immune-dependent. Allogeneic pregnancies bearing tbp,,/,, fetuses were established by either hybridizing the paternal lineage to BALB/cJ (haplotype d/d) and mating hybrid tbp,,/+ sires to haplotype b/b tbp,,/+ C57Bl/6J dams, or by transfer of haplotype b/b zygotes from tbp,,/+ × tbp,,/+ matings into pseudopregnant wild-type CByD2F1/J dams (haplotype d/d). Results, Neither hemizygous paternal allogeneic loci nor homozygous allogeneic loci, including a haplotype-mismatched major histocompatibility complex (MHC), increased abortion frequencies. Conclusion, Results suggested that mechanisms for maternal tolerance of paternal alloantigens, including mismatched MHC antigens, were intact in these pregnancies, yet maternal immune-dependent paternal antigen-independent abortion of mutants occurred. These data indicate that, in some cases of immune-mediated abortions, the presence of paternal alloantigens can be coincidental and superfluous to the compromising rejection response. [source] Placental Trophoblast from Successful Human Pregnancies Expresses the Tolerance Signaling Molecule, CD200 (OX-2),AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2003David A. Clark Problem: Th1 cytokine-dependent abortions in the CBA × DBA/2 mouse model have been linked to down-regulation of expression of the CD200 (OX-2) ,tolerance' signal on trophoblast and in decidua prior to onset of the abortion process. Abortions could be prevented by administration of a soluble CD200. Is CD200 expressed on trophoblast in successful human pregnancy? Method of study: As one cannot easily obtain trophoblasts in large quantities from successful human pregnancies in the first trimester prior to the onset of the abortion process at 6 weeks gestation, we examined as a first step, trophoblast isolated from term placentae (i.e. successful pregnancies). CD9, trophoblasts were isolated by affinity column and stained for intracellular cytokeratin, and surface CD200 using PE-anti-human CD200 monoclonal antibody. mRNA was extracted from CD9+ and CD9, cells and tested by reverse transcription,polymerase chain reaction for CD200 mRNA. CD9, placental cells were separated by velocity sedimentation and test for CD200-dependent suppression of an allogeneic human mixed lymphocyte culture where cytotoxic T cell (CTL) generation, and Th1 , Th2 cytokine production shift were measured. Results: CD9, but not CD9+ placental cell populations contained cells with mRNA for CD200, both a normal length transcript and a truncated transcript. Flow cytometry showed a CD200+ cytokeratin+ moderate-to-large-sized cell population compatible with trophoblasts and a smaller subset of cytokeratin, cells that expressed CD200 at normal and at high levels. The moderate-sized population proved most potent at inhibiting CTL generation and caused a Th1,Th2 cytokine shift. These effects were blocked by monoclonal anti-CD200. Conclusions: A subpopulation of cytokeratin+ placental trophoblasts express bioactive CD200 able to alter maternal immune responses in a favorable (Th2 > Th1) direction. Two populations of CD200+ small- and medium-small-sized cytokeratin, placental cells remain to be identified. Studies of karyotyped first trimester elective termination and spontaneous miscarriage tissues are needed. [source] | ||||||||||