Decidual T lymphocyte activation in hydatidiform mole

Department of Immunology, University of Newcastle upon Tyne, UK.
Journal of Clinical Pathology (Impact Factor: 2.92). 01/2000; 52(12):888-94. DOI: 10.1136/jcp.52.12.888
Source: PubMed

ABSTRACT To quantify and compare decidual leucocyte subpopulations in complete and partial hydatidiform molar pregnancy with those in normal early pregnancy.
Decidual leucocytes were characterised using an avidin-biotin technique and a panel of monoclonal antibodies in formalin fixed, paraffin embedded decidual tissues from 10 normal first trimester pregnancy terminations and from 13 partial and 13 complete hydatidiform moles. Immunostained cells were fully quantitated and differences between subject groups were analysed using the Mann-Whitney test. T lymphocyte populations were further characterised using double immunohistochemical labelling.
The numbers and percentages of CD3+ and CD4+ T cells were significantly increased in complete hydatidiform moles compared with partial moles and normal early pregnancy decidua. No differences were found in the number or percentage of CD8+ T cells. The CD8+ to CD4+ T cell ratio decreased significantly in complete mole compared with partial mole and normal decidua. The numbers and percentages of CD45RO+ cells increased significantly in both partial and complete hydatidiform mole compared with normal first trimester decidua. Double labelling confirmed that 50% of CD3+ T cells in complete and partial molar pregnancy coexpressed CD45RO, compared with 30% in normal pregnancy. Other leucocyte populations (eGLs, macrophages, B cells, and classical natural killer cells) did not differ between complete and partial mole and normal pregnancy decidua.
The presence of an increased population of activated decidual CD45RO+ T cells in complete and partial molar pregnancy suggests altered maternal immune responses against molar trophoblast.

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Available from: Roger Frederick Searle, Sep 29, 2015
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    • "HMs are characterized by the presence of swollen chorionic villi with Xuid accumulation, which is one of the hallmarks of inXammation. In addition, the abundance of activated decidual T cells in the endometrium of patients with the common form of HMs (Wongweragiat et al. 1999) is indicative of a dysregulated endometrial inXammation. This suggests that a dysregulated maternal inXammation of the endometrium may also be responsible for moles caused by defects in NALP7. "
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    ABSTRACT: An imprinting disorder has been believed to underlie the etiology of familial biparental hydatidiform moles (HMs) based on the abnormal methylation or expression of imprinted genes in molar tissues. However, the extent of the epigenetic defect in these tissues and the developmental stage at which the disorder begins have been poorly defined. In this study, we assessed the extent of abnormal DNA methylation in two HMs caused by mutations in the recently identified 19q13.4 gene, NALP7. We demonstrate normal postzygotic DNA methylation patterns at major repetitive and long interspersed nuclear elements (LINEs), genes on the inactive X-chromosome, three-cancer related genes, and CpG rich regions surrounding the PEG3 differentially methylated region (DMR). Our data provide a comprehensive assessment of DNA methylation in familial molar tissues and indicate that abnormal DNA methylation in these tissues is restricted to imprinted DMRs. The known role of NALP7 in apoptosis and inflammation pinpoints previously unrecognized pathways that could directly or indirectly underlie the abnormal methylation of imprinted genes in molar tissues.
    Human Genetics 11/2006; 120(3):390-5. DOI:10.1007/s00439-006-0192-3 · 4.82 Impact Factor
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    • "Thus, the interaction of the hydatiform mole with the immune system of the mother can be expected to differ from that of a normal placenta. Greater numbers of T cells, different types of T cells, and variations in T cell activation have been observed at the implantation site in hydatiform mole compared to normal pregnancy (Kabawat et al., 1985; Wongweragiat et al., 1999). However, both molar decidua (Bennett et al., 1996a) and trophoblast (Bennett et al., 1994b, 1996a; Fulop et al., 1992) produce immunosuppressive factors that may protect the mole from the maternal immune system, including an IFN--like molecule (Bennett et al., 1994a). "
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    ABSTRACT: Virtually all known cytokines have been demonstrated to be expressed in the placenta and associated fetal and maternal membranes during normal gestation. In addition to playing their traditional roles as modulators of immunological function, cytokines derived from the placenta and extraplacental membranes, together with other locally-derived growth factors, appear to be implicated in various aspects of implantation and placental development. Imbalances in the intrauterine cytokine milieu around the time of implantation and invasion may play a causative role in disorders associated with early pregnancy failure, and are also associated with the abnormal trophoblast development seen in gestational trophoblastic disease. Cytokines thus appear to be an important component of a paracrine/autocrine communication network operating within the feto-maternal interface to ensure the successful establishment of pregnancy.
    Placenta 05/2002; 23(4):239-56. DOI:10.1053/plac.2001.0781 · 2.71 Impact Factor
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