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PubMed1990

Immunology of human placental trophoblast membrane antigens.

The identification of the mechanisms of immunological survival of the semiallogeneic conceptus in utero during viviparous pregnancy is central to current studies in pregnancy immunology, since any other unmatched intrauterine allograft would be expected to suffer tissue rejection. Elucidation of normal feto-maternal interactions in human uteroplacental tissues, as well as the characterization of fetal trophoblast cell surface antigen expression, has now offered insight into these processes; these have largely focussed on the lack of trophoblastic expression of classical class I MHC antigens and the specialized local immuno-regulatory response that may occur following maternal recognition of other particular trophoblast cell surface antigens. The role of trophoblastic expression of growth factor receptors, endogenous retroviral activity and cellular oncogene products in the growth and differentiation of trophoblast, and its interaction with the host maternal tissues in early pregnancy, remains to be further clarified.

Antigens, Surface↗
PubMed1990

GZ 100, 101, 106, 107, 111, 112, 116, 121: a series of monoclonal antibodies against human trophoblast antigens.

The GZ100 series comprises a panel of monoclonal antibodies which seem to be specific for human trophoblast antigens (with the exception of GZ111, which reacts with a number of other tissues). The GZ antibodies show different reaction patterns with different trophoblast cell types. As a panel the GZ antibodies recognize all trophoblast populations (Table 2). Thus these antibodies provide a means to distinguish between trophoblast cells and maternal cells. GZ112 might be used to sort out HLA-class I positive trophoblast cells of the basal plate without blocking the HLA antigenic determinant, since GZ112 is not an anti HLA-class I antibody. At present the antigens detected by the GZ antibodies seem to be proteins, most of them with molecular weights between 50 kD and 80 kD. The function of these antigens is unclear and will be studied in future.

Animals↗
PubMed1990

Differential responses of rat trophoblast cells and embryonic fibroblasts to cytokines that regulate proliferation and class I MHC antigen expression.

TNF-alpha and type I IFN (IFN-alpha/beta) are present in the uteroplacental unit during the course of normal gestation. IFN-gamma is likely to be present during infections. To identify potential effects on two types of blastocyst-derived cells, TNF-alpha, IFN-alpha/beta, and IFN-gamma were tested for the ability to modulate proliferation and the expression of class I MHC Ag by rat trophoblast cells and embryonic fibroblasts. The three cytokines had opposite influences on cellular proliferation by the two types of cells. Growth of the trophoblast cells was inhibited by TNF-alpha, IFN-alpha/beta, and IFN-gamma, whereas both TNF-alpha and IFN-alpha/beta enhanced fibroblast proliferation. The two endogenous cytokines had different effects on class I Ag expression by trophoblast cells and fibroblasts: TNF-alpha failed to induce trophoblast cell class I Ag and IFN-alpha/beta was a poor inducer whereas fibroblast Ag were induced by both cytokines. Moreover, combinations of TNF-alpha and IFN did not increase trophoblast cell class I Ag whereas the same combinations synergized to induce class I Ag expression by fibroblasts. In contrast, IFN-gamma was a highly efficient inducer on both types of cells. The results suggest that 1) cytokines in the uteroplacental unit may orchestrate some of the events associated with placental and embryonic development by exerting differential effects on two embryologically distinct types of cells and that 2) infections may disrupt normal events.

Animals↗
PubMed1988

Expression of class I HLA genes by trophoblast cells. Analysis by in situ hybridization.

Evaluation of trophoblast cells by immunohistology has shown that subpopulations of trophoblast cells express class I HLA differently from one another and differently from embryonic and adult cells. Placental syncytial trophoblast does not express detectable levels of class I HLA; chorion membrane cytotrophoblasts bind one mAb to monomorphic determinants of class I Ag, W6/32, but not a second, 61D2. In the present study, sections of normal term placentae and matching extraplacental membranes were evaluated by in situ hybridization procedures for cells containing class I HLA mRNA using pHLA1.1, which is complementary to HLA-B. Class I Ag expression was identified by immunohistology using two mAb to class I HLA (W6/32, 61D2) and the mAb 4E to identify HLA-B. Placental syncytial trophoblast contained low to undetectable levels of class I mRNA and failed to bind all three mAb. Chorion membrane cytotrophoblast cells contained moderate levels of class I HLA mRNA and were positive with the mAb W6/32 but were negative with 61D2 and 4E. In adjacent tissues, fetal mesenchymal cells and maternal decidual cells contained high levels of class I mRNA and were positive with all three mAb. The results suggest that syncytial trophoblast may not express class I HLA because of low steady-state levels of class I HLA mRNA. In contrast, chorionic cytotrophoblast cells may express truncated versions of class I HLA or nonclassical HLA-A,B,C-like Ag. Regulation of the expression of class I HLA gene products may be essential to the development of a satisfactory immunologic relationship between the mother and her semiallogeneic fetus during pregnancy.

Antibodies, Monoclonal↗
PubMed1989

Clinical experience with trophoblastic diseases in Nepal.

The epidemiology of trophoblastic disease in Nepal remains unknown. In this study, the first data regarding patients with trophoblastic disease were collected from two hospitals in Kathmandu, Nepal. We found 68 molar pregnancies during 1986 to 1987 at the Maternity Hospital, there. The incidence of molar pregnancies during two years ranged 2.84 per 1000 pregnancies and 3.24 per 1000 deliveries, while the total number of trophoblastic diseases from 1985 to 1988 at Teaching Hospital, Tribhuvan University, Kathmandu, numbered 26. The incidence of trophoblastic disease ranged from 7.07 per 1000 pregnancies to 8.04 per 1000 deliveries. As a result, the rate of trophoblastic disease in Nepal seems to be higher than expected, and it indicates a incidence similar to that other Asian countries at sea level.

Adult↗
PubMedDate not supplied

Pulmonary trophoblastic deportation. Cytologic aspects.

In the present paper the human pulmonary trophoblastic deportation was studied in 180 sputum specimens from 90 pregnant, parturient and puerperal patients. The syncytial trophoblastic cells were searched in the sputum with the Papanicolaou and Shorr techniques. The morphology of the isolated syncytial trophoblastic cells was studied in placental imprints and compared with isolated megakaryocytes in bone marrow smears. The data in the literature and our own results suggest that the absence of syncytial trophoblastic cells in the sputum from pregnant, parturient and puerperal patients may be due to the following factors: (a) all the patients were normal; (b) the syncytial trophoblastic cells degenerate in the pulmonary capillaries and therefore do not reach the alveoli; (c) the specimens were collected without any special technique. This investigation must be carried out in abnormal conditions of "placental commotion" such as eclampsia, caesarian section, uterine manipulation, etc.

Adolescent↗
PubMed1989

[Immunohistochemical analysis of the expression of HLA on the trophoblast of normal pregnancy].

The expression of MHC class II antigens (HLA-DR, -DP, -DQ) on trophoblast was analyzed by an immunoperoxidase technique using monoclonal antibodies. Tissues were obtained after pregnancy hysterectomy with the medical indications and after normal deliveries. They were snap-frozen in liquid nitrogen, cut in a cryostat and fixed in acetone for 10 minutes. Mouse monoclonal antibodies used in this study were anti-HLA-ABC (W6/32, Sera lab), anti-HLA-DR (Cappel), anti-HLA-DP (B7/21, Becton Dickinson) and anti-HLA-DQ (anti-Leu-10, Becton Dickinson) in addition to anti-cytokeratin (CAM5.2, Becton Dickinson) to recognize trophoblast. In the first trimester, HLA-DP could be identified on cytotrophoblastic cell column, cell island, extravillous trophoblast invading the decidua basalis, which were positive for HLA-ABC, and villous cytotrophoblast. In term placenta, villous syncytiotrophoblast and extra-villous trophoblast found in the decidua were positive for HLA-DP. In contrast, no trophoblast reacted with anti-HLA-DR or anti-HLA-DQ.

Antibodies, Monoclonal↗
PubMed1985

Clinical and laboratory investigation of a virilized woman with placental-site trophoblastic tumor.

The novel association of virilization and placental-site trophoblastic tumor, an uncommon form of gestational trophoblastic disease (formerly called "trophoblastic pseudotumor"), is described in a 32-year old woman. Multiple agent chemotherapy lowered serum concentrations of chorionic gonadotropin (hCG) (8.7 to 2.1 ng/mL), pregnancy-specific beta 1-glycoprotein (32 to 3.9 ng/mL), and testosterone (400 to 74 ng/dL). Subsequent hysterectomy revealed a 2-cm tumor nodule within the myometrium, and one week postoperatively serum concentrations of hCG (0.5 ng/mL), pregnancy-specific beta 1-glycoprotein (1.3 ng/mL), and testosterone (20 ng/dL) had all returned to normal. Percutaneous catheterization of the ovarian veins before chemotherapy demonstrated a 50-fold elevation of ovarian vein testosterone concentrations compared with normal women, whereas ovarian vein 17 beta-estradiol concentrations were only twofold higher than normal. Direct sampling of the uterine veins at the time of hysterectomy documented testosterone and estradiol production, presumably by the placental-site trophoblastic tumor. Ovarian vein testosterone concentrations at this time were only fourfold above normal, probably the result of falling serum concentrations of hCG. Wedge biopsy of the ovaries disclosed minimal histologic changes (thecal cell luteinization, focal thecosis) compatible with hCG stimulation. Failure of the placental-site trophoblastic tumor to produce large amounts of estrogen, in contrast to normal pregnancy and hydatidiform mole, resulted in marked androgen/estrogen imbalance, high circulating concentrations of free testosterone, and virilization.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Ultrastructural morphometric analysis of Brucella abortus-infected trophoblasts in experimental placentitis. Bacterial replication occurs in rough endoplasmic reticulum.

Trophoblasts in normal and Brucella abortus-infected caprine placentas were examined by ultrastructural morphometric analysis to establish structural relationships of B abortus with cytoplasmic organelles; brucellae were identified with colloidal gold-labeled anti-B abortus bovine IgG. Cytotrophoblasts had large numbers of B abortus in cisternae of rough endoplasmic reticulum; binucleate trophoblasts did not contain bacteria. In infected trophoblasts there was a significant hypertrophy of B abortus-filled rough endoplasmic reticulum (RER) and a corresponding reduction in normal-appearing RER. Volume and surface density of RER in trophoblasts were: normal placentas (control), 2.8% and 0.30 sq mu; infected placentas, 27.9% (27.4% of which contained B abortus) and 0.56 sq mu (cells containing B abortus) and 3.3% and 0.34 sq mu (cells not containing B abortus). These data suggest that B abortus replicates within the RER of trophoblasts, possibly for synthesis and glycosylation of bacterial membrane proteins.

Animals↗
PubMed1979

Trophoblast growth in the lungs of mice.

Trophoblast giant cells grow from ectoplacental cones of 7 1/2 days' gestation that are implanted in the lung from the surface, intrabronchially, or via the circulation. When blastocysts of 3 1/2 days' gestation are implanted in lung, their behavior varies according to the route of implantation and the ages of the recipient mice. Blastocysts produced trophoblast giant cells when implanted in the bronchial tree. Trophoblast giant cells were not seen in adult lungs when blastocysts were introduced via the circulation. However, they were seen in 12-day-old mice injected in the same way 10 days previously. Something is apparently liberated from adult lung vessels which interacts with the blastocyst or zona pellucida and causes rapid degeneration of trophoblast. Experiments designed to extract this agent are in progress in the hope that the agent may be useful in the treatment of human trophoblastic disease.

Animals↗
PubMed1985

Effect of acetylsalicylic acid on prostacyclin production in trophoblast.

In attempt to elucidate whether acetylsalicylic acid (ASA) has an in vivo effect on prostacyclin (PGI2)-like activity released from trophoblast we have evaluated PGI2-like activity in pregnant women scheduled for pregnancy termination after ASA ingestion. Following subjects were studied: Group I: 7 healthy pregnant women who were treated with 1.5 g ASA for two days; Group II: 18 control pregnant women who received placebo for two days. Trophoblast specimens were obtained by legal abortions; PGI2-like activity in trophoblast was measured by the method of Moncada. In normal pregnant women (8-10 weeks gestation) treated with ASA the mean PGI2-like activity of trophoblast significantly decreased compared to the controls. These data indicate that treatment with ASA of early pregnant women might have a harmful effect on trophoblast and the problem should be further explored before allowing the administration of cyclooxygenase inhibiting drugs during early pregnancy.

Adult↗
PubMed1966

Trophoblastic disease. Concepts of management.

Trophoblastic tumors are a notoriously unpredictable group in which metastasis may occur from histologically benign tumors and cause death, whereas a histologically malignant tumor may spontaneously disappear. Additional problems are created by the inability to accurately establish a diagnosis before abortion of molar tissue or development of metastasis.In recent years chemotherapy has dramatically improved the prognosis of patients with choriocarcinoma. This fact, plus the importance of the time interval between onset of disease and the beginning of chemotherapy, makes close follow-up of patients with trophoblastic tumors imperative.Concepts of therapy for trophoblastic tumors are rapidly changing. Indications for chemotherapy are broadening, especially in the areas of persistent and metastatic trophoblastic disease. As surgical intervention in the form of hysterectomy is becoming less important, the reproductive capacity of these young women is being preserved. Astute diagnosis, appropriate therapy and active life-long follow-up are the essentials in the management of patients with trophoblastic disease.

Adult↗
PubMed1979

[Plication of the nuclear membrane and its derivatives in the polyploid cell nuclei of the rat trophoblast].

Folding pattern of the nucleus envelope and intranuclear membrane structures in trophoblast giant cells and in trophoblast of the intermediate region of the rat placenta have been studied. Cells of the intermediate region of the placenta demonstrate deep invaginations resulting in the appearance of lobulated nuclei. Invaginations of the nuclear envelope pass on a narrow fold made by an inner nuclear membrane. The polyploid nuclei of trophoblast giant cells have superficial folds and deeper finger-like invaginations in their envelopes. Such folding trophoblast nuclei in two populations examined are met throughout the whole ontogenesis of the cell. In the giant cells, individual intranuclear tubes or their accumulations are seen. The tubes are made by a unit membrane and are surrounded with a matrix. The nuclear chromatin, diffuse or condenced, is in association with the tube surface. The tubes are met near the nucleolus and on its surface, where these are surrounded with the granular component of the nucleolus. In the trophoblast of the intermediate region of the placenta, intranuclear concentric membranes have been found; made of paired membranes, intramembranous space being filled with electron dense matrix. The concentric membranes lie separately in the karyoplasm, not being associated with the chromatin.

Animals↗
PubMed1984

The hCG assay in the treatment of trophoblastic disease.

The most important criterion in monitoring the treatment of patients with trophoblastic disease is the quantitative measurement of hCG levels. It is particularly important to have a sensitive hCG-detection procedure that reliably distinguishes low positive hCG levels from negative ones. Reliable monitoring of serum hCG levels minimizes unnecessary chemotherapy in patients entering remission and provides an early indication for additional chemotherapy if and when the hCG levels again become detectable. We evaluated a two-site monoclonal-antibody immunoradiometric assay (IRMA) for its reliability in the management of trophoblastic disease. The assay utilizes a solid-phase, monoclonal antibody that recognizes the alpha subunit of complete hCG and a 125I monoclonal antibody that recognizes the beta subunit. The minimal effective concentration of hCG detectable with the IRMA is 3-4 mIU/ml. The study population consisted of 6 choriocarcinoma patients, 49 hydatidiform mole patients, 37 patients being monitored after spontaneous abortion or blighted ovum and 80 patients in whom the possibility of trophoblastic disease was being ruled out. Each serum specimen was analyzed with the IRMA and in one or more of a number of different radioimmunoassays. The results were correlated with the patient's clinical course. Of the procedures evaluated, the IRMA was the most reliable in identifying trophoblastic-disease patients who required additional chemotherapy. Furthermore, the IRMA yielded no persistent low positive hCG values in patients without clinical evidence of trophoblastic disease. Therefore, the two-site IRMA is recommended for accurately distinguishing a clinically relevant low positive hCG level from an undetectable one.

Choriocarcinoma↗
PubMed1982

Identification of human trophoblast membrane antigens in maternal blood during pregnancy.

The development of an immunoradiometric assay for the detection of human trophoblast-specific membrane antigens is described. The test revealed for the first time circulating trophoblast-specific cell membrane antigens in the peripheral blood of pregnant women, but none in non-pregnant female or male controls. Comparison of the circulating levels of these trophoblast-specific proteins between normal and pre-eclamptic blood samples showed no significant differences, thus casting doubt on the role of differential trophoblast antigen deportation in the etiology of toxaemic pregnancy. Matched retroplacental cord blood from several normal and pre-eclamptic pregnancies were examined and found either negative or near the lower sensitivity limit of the assay, suggesting that deportation of trophoblast membrane antigens during gestation is limited to the maternal aspect of the placenta.

Antigens, Surface↗
PubMed1982

[Diagnosis, prevalence, prognosis and treatment of the trophoblastic component in germinal tumours of the testis in the adult].

The authors report a series of 97 germinal tumours of the testis in the adult, studied first in terms of conventional histological data. Of 33 seminomas, 2 secreted HCG. The 5-year actuarial survival at stage I was 93%, and at stage II 75%. Stage II deaths revealed the existence of not purely seminomatous tumours. Amongst dysembryomas, half secreted HCG, with 3 histological groups: predominant choriocarcinomas, tumours with a trophoblastic component and "apparently pure" dysembryomas. The 3-year actuarial survival for dysembryomas was 90% at stage I and 58% at stage II. 51 patients of the series were studied retrospectively by sections with HCG peroxidase, a technique which reveals the intracytoplasmic synthesis of the hormone. Two types of cells have proved capable of such synthesis: syncytial cells, of syncytial-trophoblastic type, and small mononuclear cells. One third of seminomas and 90% of dysembryomas proved to have a trophoblastic component as demonstrated by HCG immunoperoxidases. All patients secreting HCG were HCG peroxidase positive. This equally applied to all patients with syncytial cells. Furthermore, all the indications are that HCG secretion is above all by the syncytial cells. From a diagnostic standpoint, any rise in beta HCG is synonymous with an HCG immunoperoxidase trophoblastic component. Detection of such a component using immunoperoxidase would seem to be essential for non-secreting tumours. From a prognostic standpoint, seminomas with a trophoblastic component are in fact dysembryomas and lymph node dissection should be performed, this being the only way of not missing a non-seminomatous metastasis. Therapeutically, pure seminomas are distinguished by the possibility of cure by radiotherapy. For all other tumours, orchidectomy must be followed by lymph node dissection. Subsequent treatment is decided on the basis of the results of the latter, with the exception of tumours with visceral metastases where chemotherapy must come first.

Adult↗
PubMed1984

[Role of hysteroscopy in diagnosis and management of trophoblastic disease].

To confirm complete removal of trophoblastic tissues, hysteroscopy was performed in 21 patients after evacuation of hydatidiform mole with an interval of a week. In 15 of these cases, hysteroscopy employed within a week after evacuation of the mole revealed a residue of mole or necrotic decidua. Although complete removal was confirmed in 14 cases on the second hysteroscopy, re-curettage was necessary in 6 patients because necrotic tissues were still found in the uterine cavity. Possible diagnosis of invasive mole was made in 2 cases within 2 weeks after evacuation of the mole by hysteroscopic findings. Hysteroscopy was also performed in 27 patients who were suspected of having a trophoblastic disease from the clinical signs and urinary hCG titer. Hysteroscopic findings which suggested trophoblastic diseases were summarized in the following four categories; 1) the existence of vesicles, 2) buldging or 3) recess of the uterine wall with bleeding or dilated blood vessels and 4) hematoma of the uterine wall. In 9 of the 21 cases with choriocarcinoma, invasive mole or persistent trophoblastic disease, one or two of the above mentioned findings were noted. Moreover, it was possible to differentiate syncytial endometritis from trophoblastic disease from the hysteroscopic findings. Therefore, hysteroscopy seems to be a useful aid not only in confirming complete evacuation of hydatidiform mole but also in the diagnosis and management of malignant sequela.

Chorionic Gonadotropin↗
PubMed1982

Detection of IgG bound within human trophoblast.

Previous studies have failed consistently to detect either binding sites for exogenous IgG or endogenous IgG on human trophoblast by using conventional immunohistologic methods. The present study demonstrates specific binding sites for exogenous IgG on all trophoblast-derived cells. The binding sites were detectable with monomeric IgG but not IgG aggregates. The binding sites were detected more easily if cells were washed at an acid pH (5.0). The level of binding activity was greater in younger placental tissue, although expression of binding sites on cells in extraplacental membranes was age-independent. Complexing of bound exogenous IgG resulted in its dissociation from tissue binding sites. Endogenous trophoblast-associated IgG was readily detectable when anti-IgG reagents that produced minimal complexing were used, e.g., Fab fragments of rabbit antihuman IgG. High levels of both Fc gamma binding sites and endogenous IgG were detected in placentae as late as 30 wk gestation, but both were present only in low levels at term. The results demonstrate that both binding sites for exogenous and endogenous IgG are associated with the human trophoblast and support the theory that IgG transport through the human trophoblast is dependent on Fc gamma receptors.

Female↗