PubMed Health⌕ Search

Biomedical subjects

W A Bennett

Publications and source records attributed to W A Bennett.

At least 19 recordsLinked to original sources
PubMed2001

Interleukin-10 administration and bacterial endotoxin-induced preterm birth in a rat model.

OBJECTIVE: To determine whether intra-uterine infusion of interleukin-10 prevents preterm delivery in rats treated with endotoxin. METHODS: Pregnant rats underwent implantation of uterine catheters and were randomly assigned to receive intrauterine infusion of either normal saline, 50 microg lipopolysaccharide endotoxin, or 50 microg lipopolysaccharide with 500 ng interleukin-10 administered either concurrently or 24 hours later. The interval from infusion to delivery for each group was recorded, along with the number of live born pups and their birth weight. We calculated that to obtain a power of 80%, assuming a 24-hour difference in the treatment to delivery times between the test and control subjects, at least six animals would be needed in each group. RESULTS: In females receiving lipopolysaccharide (50 microg) alone, the interval to delivery (P <.05), live birth rate (P <.05), and pup weight (P <.001) were reduced compared with the saline-infused controls. In contrast, females receiving interleukin-10 at the time of the endotoxin challenge or 24 hours after delivered at term with no difference in litter size or live birth weight compared with the controls. CONCLUSION: Animals treated with both lipopolysaccharide and interleukin-10, administered concurrently or 24 hours after the endotoxin challenge, delivered normal weight pups at term with a similar litter size as the saline-infused controls. Interleukin-10 appears to be effective in preventing endotoxin-induced preterm birth and fetal wastage in pregnant rats.

Animals↗
PubMed2001

Pathophysiology of pregnancy-induced hypertension.

Pregnancy-induced hypertension (PIH) is estimated to affect 7% to 10% of all pregnancies in the United States. Despite being the leading cause of maternal death and a major contributor of maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of PIH have not yet been fully elucidated. Studies during the past decade, however, have provided a better understanding of the potential mechanisms responsible for the pathogenesis of PIH. The initiating event in PIH appears to be reduced uteroplacental perfusion as a result of abnormal cytotrophoblast invasion of spiral arterioles. Placental ischemia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium that results in enhanced formation of endothelin and thromboxane, increased vascular sensitivity to angiotensin II, and decreased formation of vasodilators such as nitric oxide and prostacyclin. The quantitative importance of the various endothelial and humoral factors in mediating the reduction in renal hemodynamic and excretory function and elevation in arterial pressure during PIH is still unclear. Investigators are also attempting to elucidate the placental factors that are responsible for mediating activation/dysfunction of the maternal vascular endothelium. Microarray analysis of genes within the ischemic placenta should provide new insights into the link between placental ischemia and hypertension. More effective strategies for the prevention of preeclampsia should be forthcoming once the underlying pathophysiologic mechanisms that are involved in PIH are completely understood.

Blood Pressure↗
PubMed2001

Role of neuronal nitric oxide synthase in mediating renal hemodynamic changes during pregnancy.

Renal plasma flow (RPF) and glomerular filtration rate (GFR) are markedly increased during pregnancy. We recently reported that the renal hemodynamic changes observed during pregnancy in rats are associated with enhanced renal protein expression of neuronal nitric oxide synthase (nNOS). The purpose of this study was to determine the role of nNOS in mediating renal hemodynamic changes observed during pregnancy. To achieve this goal, we examined the effects of the nNOS inhibitor 7-nitroindazole (7-NI) on kidney function in normal conscious, chronically instrumented virgin (n = 6) and pregnant rats (n = 9) at day 16 of gestation. Infusion of 7-NI had no effect on RPF (4.7 +/- 0.7 vs. 4.8 +/- 0.9 ml/min), GFR (2.2 +/- 0.2 vs. 2.5 +/- 0.4 ml/min), or mean arterial pressure (MAP; 127 +/- 7 vs. 129 +/- 10 mmHg) in virgin rats. In contrast, 7-NI infused into pregnant rats decreased RPF (8.9 +/- 1.6 vs. 6.5 +/- 1.4 ml/min) and GFR (4.4 +/- 0.7 vs. 3.3 +/- 0.7 ml/min) while having no effect on MAP (123 +/- 4 vs. 123 +/- 3 mmHg). In summary, inhibition of nNOS in pregnant rats at midgestation results in significant decreases in RPF and GFR. nNOS inhibition in virgin rats had no effect on renal hemodynamics. These data suggest that nNOS may play a role in mediating the renal hemodynamic changes that occur during pregnancy.

Animals↗
PubMed2001

Endothelin type a receptor blockade attenuates the hypertension in response to chronic reductions in uterine perfusion pressure.

A chronic reduction in uterine perfusion pressure in pregnant rats is associated with a significant elevation in mean arterial pressure (MAP) and reduction in kidney function. The purpose of this study was to examine the role of endothelin in mediating the hypertension in response to chronic reductions in uterine perfusion pressure in conscious, chronically instrumented, pregnant rats. MAP in pregnant rats with chronic reductions in uterine perfusion pressure (123.0+/-1.8 mm Hg) was significantly higher than that in control pregnant rats (101.3+/-4.0 mm Hg). Renal expression of preproendothelin mRNA as determined by ribonuclease protection assay was also significantly elevated in the medulla (>45%, P<0.05) and in the cortex (>22%, P:<0.05) of the pregnant rats with chronic reductions in uterine perfusion pressure compared with control pregnant rats. Chronic administration of the selective endothelin type A receptor antagonist (ABT-627, 5 mg/kg per day for 10 days) markedly attenuated the increase in MAP observed in the pregnant rats with chronic reductions in uterine perfusion pressure (103.3+/-5.6 mm Hg, plus endothelin antagonist; P<0.05). However, endothelin type A receptor blockade had no significant effect on blood pressure in the normal pregnant animals (96.0+/-2.7 mm Hg, plus endothelin antagonist). These findings suggest that endothelin plays a major role in mediating the hypertension produced by chronic reductions in uterine perfusion pressure in pregnant rats.

Animals↗
PubMed2001

Reduced uterine perfusion pressure during pregnancy in the rat is associated with increases in arterial pressure and changes in renal nitric oxide.

A reduction in nitric oxide (NO) synthesis has been suggested to play a role in pregnancy-induced hypertension. We have recently reported that normal pregnancy in the rat is associated with significant increases in whole-body NO production and renal protein expression of neuronal and inducible NO synthase. The purpose of this study was to determine whether whole-body and renal NO production is reduced in a rat model of pregnancy-induced hypertension produced by chronically reducing uterine perfusion pressure starting at day 14 of gestation. Chronic reductions in uterine perfusion pressure resulted in increases in arterial pressure of 20 to 25 mm Hg, decreases in renal plasma flow (<23%) and glomerular filtration rate (<40%), but no difference in urinary nitrite/nitrate excretion relative to control pregnant rats. In contrast, reductions in uterine perfusion pressure in virgin rats resulted in no significant effects on arterial pressure. Renal endothelial (<4%) and inducible (<11%) NO synthase protein expression did not decrease significantly in the chronically reduced uterine perfusion pressure rats relative to normal pregnant rats; however, significant reductions in neuronal NO synthase were observed (<30%). The results of this study indicate that the reduction in renal hemodynamics and the increase in arterial pressure observed in response to chronic decreases in uterine perfusion pressure in pregnant rats are associated with no change in whole-body NO production and a decrease in renal protein expression of neuronal NO synthase.

Animals↗
PubMed2001

Pathophysiology of hypertension during preeclampsia linking placental ischemia with endothelial dysfunction.

Studies over the past decade have provided a better understanding of the potential mechanisms responsible for the pathogenesis of preeclampsia. The initiating event in preeclampsia has been postulated to be reduced uteroplacental perfusion as a result of abnormal cytotrophoblast invasion of spiral arterioles. Placental ischemia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium that results in enhanced formation of endothelin and thromboxane, increased vascular sensitivity to angiotensin II, and decreased formation of vasodilators such as NO and prostacyclin. These endothelial abnormalities, in turn, cause hypertension by impairing renal-pressure natriuresis and increasing total peripheral resistance. The quantitative importance of the various endothelial and humoral factors in mediating the reduction in renal hemodynamic and excretory function and elevation in arterial pressure during preeclampsia are still unclear. Results from ongoing basic and clinical studies, however, should provide new and important information regarding the physiological mechanisms responsible for the elevation in arterial pressure in women with preeclampsia.

Blood Pressure↗
PubMed2000

Intrauterine endotoxin infusion in rat pregnancy induces preterm delivery and increases placental prostaglandin F2alpha metabolite levels.

OBJECTIVE: This study was designed to examine the effects of intrauterine endotoxin (lipopolysaccharide) on rat pregnancy. STUDY DESIGN: Pregnant Sprague-Dawley rats (N = 26) were implanted with uterine catheters on day 15 or 16 of a 22-day gestation. Animals were randomly assigned to receive either lipopolysaccharide (25 or 50 microg) or sodium chloride solution (1 mL) on day 17 and then were either sacrificed on day 19 or observed until delivery. Placentas were harvested at the time of death, homogenates were prepared, and prostaglandin F(2)(alpha) metabolite levels were determined by means of radioimmunoassay. Data were analyzed by analysis of variance, Student-Newman-Keuls, and Mann-Whitney tests. RESULTS: Lipopolysaccharide-treated groups (25 and 50 microg) displayed a shorter interval to delivery (mean +/- SE, 82 +/- 13 and 63 +/- 8 hours, respectively) than control animals (117 +/- 3 hours). Pups of lipopolysaccharide-treated (25 and 50 microg) female animals had lower live birth weights (4.92 +/- 0.01 and 5.12 +/- 0. 24 g, respectively) compared with control animals (6.04 +/- 0.07 g). Placental homogenates from lipopolysaccharide-treated female animals contained higher levels of prostaglandin F(2)(alpha) metabolite (1567 +/- 64 and 1475 +/- 59 pg/mL) than those from sodium chloride solution-infused control animals (804 +/- 68 pg/mL). CONCLUSION: Bacterial products induce the preterm delivery of low-birth-weight pups in rats, possibly by increasing local prostaglandin biosynthesis.

Animals↗
PubMed1999

Expression of the placental cytokines tumor necrosis factor alpha, interleukin 1beta, and interleukin 10 is increased in preeclampsia.

OBJECTIVE: We sought to determine whether placental cytokine expression is altered in patients with preeclampsia. STUDY DESIGN: Whole placental tissue was collected at cesarean delivery, and total ribonucleic acid was extracted. Reverse transcriptase-polymerase chain reaction was performed to determine cytokine expression. Product bands were quantitated by scanning densitometry, and results were expressed as a ratio of cytokine/housekeeping gene (cytokine expression index). Statistical analysis was performed by the Student t test and the Mann-Whitney U test. RESULTS: Placentas from 6 patients with preeclampsia and 4 normotensive patients were analyzed. Placental expression of interleukin 1beta and interleukin 10 was greater in preeclamptic women than in normotensive subjects (median interleukin 1beta cytokine expression index, 0.675; range, 0.394-0. 953; vs 0.106; range, 0.084-0.166; P =.011; median interleukin 10 cytokine expression index, 1.042; range, 0.672-1.192; vs 0.126; range, 0.062-0.398; P <.011). Tumor necrosis factor alpha messenger ribonucleic acid was detected in placentas of preeclamptic subjects but not in normotensive control subjects. CONCLUSION: Placentas from preeclamptic patients demonstrated increased expression of interleukin 1beta, interleukin 10, and tumor necrosis factor alpha. This may be in association with placental hypoxia and may contribute to the global endothelial dysfunction observed in preeclampsia.

Adult↗
PubMed1999

First-trimester human chorionic villi express both immunoregulatory and inflammatory cytokines: a role for interleukin-10 in regulating the cytokine network of pregnancy.

PROBLEM: T-helper 2 (TH2)-type cytokines [i.e., interleukin (IL)-6, IL-10, and IL-13] and transforming growth factor (TGF)-beta are expressed by the murine decidua and/or placenta and are likely to suppress inflammatory cytokine [i.e., IL-2, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, IL-1 alpha, and IL-1 beta] production at the maternal-fetal interface. In addition, class I IFNs may protect the fetus from immunologic rejection and viral infections. This study examines the expression of inflammatory/immunoregulatory cytokines and IL-10 production by first-trimester chorionic villi. METHOD OF STUDY: Gestational tissues (n = 5) were obtained following elective terminations performed between 7 and 9 weeks of gestation. Chorionic villous tissues were separated from fetal membranes and decidua, and total RNA was extracted. Cytokine expression was assessed by a reverse transcriptase-polymerase chain reaction technique. Chorionic villi (n = 9; 6-12 weeks gestation) were maintained in organ culture, and human chorionic gonadotropin (hCG) and IL-10 levels were determined by immunoradiometric and enzyme-linked immunosorbent assays, respectively. RESULTS: IFN-gamma and IL-2 were generally not expressed by first-trimester chorionic villi. Low to moderate levels of expression were noted for IL-1 alpha, IL-1 beta, and TNF-alpha. High levels of mRNA were noted for IFN-alpha and IFN-beta, but IFN-tau was not expressed. In all tissues, TGF-beta 1 and IL-13 were either weakly expressed or not expressed. In contrast, moderate to high levels of IL-6 and IL-10 mRNA were detected in each chorionic villous sample. In chorionic villous explants obtained at 6-11 weeks gestation production of hCG and IL-10 was greatest during the first 24 hr ([hCG] = 6961 +/- 815 mIU/mL, [IL-10] = 92 +/- 11 pg/mL) and then declined through 72 hr. CONCLUSIONS: TH1-type cytokines (IL-2, IFN-gamma) are not expressed by first-trimester chorionic villous tissues: This is possibly due to local production of IL-10. In contrast, macrophage-associated cytokines (IL-1 beta and TNF-alpha) are expressed and their regulation may be critical for fetal survival. Finally, class 1 IFNs expressed by early chorionic tissues may protect the fetus from maternal rejection and viral transmission.

Abortion, Induced↗
PubMed1998

Cytokine expression by first-trimester human chorionic villi.

PROBLEM: Communication at the human maternal-fetal interface occurs by an intricate cytokine network. This study examines cytokine expression by normal first-trimester human chorionic villi. METHOD OF STUDY: Tissues were obtained at elective pregnancy terminations (7-9 weeks). Total RNA was isolated from chorionic villi by guanidinium isothiocynate-acid phenol extraction. A reverse transcriptase-polymerase chain reaction technique was used to examine cytokine expression. beta-Actin was used as the housekeeping gene, and mitogen-stimulated lymphocytes served as positive controls. RESULTS: beta-Actin was uniformly expressed by all chorionic villous samples. Interferon (IFN)-alpha and -beta also were highly expressed. Moderate expression was noted for interleukin (IL)-10, IL-6, tumor necrosis factor (TNF)-alpha, and IL-1 beta. In contrast, transforming growth factor-beta 1, IFN-gamma, IL-2, and IL-1 alpha were either weakly expressed or absent in first-trimester villi. CONCLUSIONS: Cytokines may contribute to pregnancy immunotolerance (IFN-alpha, IFN-beta, and IL-10), viral resistance (IFNs), hormone secretion (IL-1 and IL-6), and cellular remodeling (IFN-gamma and TNF-alpha) within the chorionic villous.

Adjuvants, Immunologic↗
PubMed1997

Expression and production of interleukin-10 by human trophoblast: relationship to pregnancy immunotolerance.

Interleukin-10 (IL-10) is a T-helper type-2 (Th2) cytokine noted for its ability to suppress cytokine synthesis by T-helper type-1 (Th1) cells. IL-10 may play a role in pregnancy immunotolerance through the establishment of a Th2 cytokine bias at the maternal-fetal interface. This study examines the expression and production of IL-10 by normal and malignant human trophoblast. Term placental biopsies, cloned choriocarcinoma cell lines and isolated human trophoblast were utilized for the study of IL-10 expression. Choriocarcinoma cells (BeWo, JEG-3, JAR) were maintained in T-flask culture until confluence and then harvested by enzymatic dispersion. Purified term trophoblast were obtained by sequential trypsin/DNAse digests and CD9 immunoaffinity chromatography. Amplified IL-10 mRNA was detected by a reverse transcriptase polymerase chain reaction (RTPCR) technique. BeWo cells were maintained in artificial capillary culture (ACC) and conditioned media assayed for IL-10. Granulocyte macrophage-colony stimulating factor (GM-CSF; 1.0, 10.0 and 100.0 ng/ml) was added to the BeWo cultures to examine its effects on trophoblast IL-10 production. IL-10 determinations were performed using a human ELISA system. IL-10 mRNA was detected in each trophoblast cell type examined with the exception of the JEG-3 choriocarcinoma cell line. IL-10 protein was also detected (range 6-22 pg/ml) in BeWo media on days 8 to 11 of culture. When serum was reduced in the culture media, IL-10 levels fell below the sensitivity of the assay (5 pg/ml). Subsequent addition of GM-CSF stimulated BeWo IL-10 secretion in a dose-related fashion. These results support the concept IL-10 is expressed at the human maternal-fetal interface, and production of this important immunoregulatory molecule may be regulated, in part, by GM-CSF.

Antibodies, Monoclonal↗
PubMed1996

Comparison of immunosuppressive properties of hydatidiform mole decidua and trophoblast extracts.

PROBLEMS: The immunologic privilege afforded the fetus relies upon immunoregulation within the maternal-fetal interface. Trophoblast and decidua-derived immunoregulatory factors enforce this privilege by locally suppressing maternal responses to trophoblast antigens. The relative contribution of trophoblast or decidua immunosuppressive factors to pregnancy immunotolerance are not well characterized. The purpose of this study was to compare the suppressive effects of hydatidiform mole trophoblast and decidua extracts on interleukin-2-dependent proliferation. METHOD: Tissue extracts were prepared from hydatidiform mole trophoblast and decidua following uterine evacuation. Samples were submitted to interleukin-2-dependent and -independent cell proliferation assays. RESULTS: Hydatidiform mole trophoblast extract significantly (P < 0.05) suppressed interleukin-2-dependent proliferation but did not affect interleukin-2-dependent cell proliferation. In contrast, molar decidua extract suppressed both cell lines. CONCLUSIONS: Human hydatidiform mole trophoblast contains factor(s) that specifically abrogate interleukin-2-dependent clonal expansion of murine cytotoxic T-cells. In contrast, extracts of molar decidua suppressed both interleukin-2-dependent and -independent responses. This indicates that the trophoblast antagonizes critical interleukin-2-mediated immunologic responses, but that the decidua uses nonspecific antiproliferative mechanisms for immunoregulation.

Decidua↗
PubMed1996

Cytokine expression by models of human trophoblast as assessed by a semiquantitative reverse transcription-polymerase chain reaction technique.

PROBLEM: Cytokines form an important communication network between the mother and fetus. Defining the significance of these factors requires an understanding of their constitutive expression by maternal and fetal tissues. This study examines cytokine expression by human trophoblast. METHODS: A reverse transcription polymerase chain reaction (RT-PCR) technique was used to assess cytokine expression by choriocarcinoma cells (BeWo, JEG-3, and JAR) and term trophoblast. Placental digests were enriched for trophoblast by immunoaffinity (CD-9) columns. RESULTS: Interleukin (IL)-1, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma were weakly expressed or absent in the choriocarcinoma cells. In contrast, these cytokines were expressed by term trophoblast. IL-6, IL-10, IFN-alpha, IFN-beta, and granulocyte macrophage-colony stimulating factor (GM-CSF) mRNA were detected in all trophoblast cells, except for a paucity of IL-10 expression by JEG-3 cells. CONCLUSIONS: Human choriocarcinoma cells and term trophoblast express cytokines that may regulate critical reproductive events. Expression of inflammatory cytokines such as IL-1, TNF-alpha, and IFN-gamma by term trophoblast could trigger labor or be a consequence of labor-associated events.

Cell Line↗
PubMed1995

Immunosuppression by conditioned media derived from a cloned choriocarcinoma cell line in serum-supplemented and defined media.

PROBLEM: Immunosuppressive factor(s) of trophoblast origin may contribute to the immunological privilege afforded the fetal allograft. Characterization of these immunoregulators in humans has been impeded by a lack of sufficient quantities of early gestational trophoblast for experimentation. METHOD: In this study, a cloned choriocarcinoma cell line (BeWo) was evaluated as an experimental model of trophoblast-derived immunoregulation. BeWo cells were cultured in both serum-supplemented (15% fetal bovine serum; FCS-CM) and serum-free (10% bovine serum albumin, BSA-CM; 0.01% gelatin, Gel-CM) media. Immunosuppressive activity was determined through the use of interleukin-2-dependent (CTLL-2) and -independent (LBRM) cell lines. Human chorionic gonadotropin (hCG) levels were determined by an immunoradiometric assay, and cellular morphology was assessed by light microscopy. RESULTS: In the serum-supplemented cultures, a portion of cells underwent transformation from single nucleated cytotrophoblast to multinucleated syncytiotrophoblast during days 1 to 5 of culture and was accompanied by a rise in hCG. Serum-free cultures were characterized as islands of cytotrophoblast and did not exhibit differentiation. FCS-CM suppressed CTLL-2 and LBRM proliferation with estimated EC50 values of 415 and 280 micrograms protein/mL, respectively. Gel-CM suppressed CTLL-2 and LBRM proliferation with EC50 values of 12 and 7 micrograms protein/mL, respectively. BSA-CM suppressed CTLL-2 proliferation with an EC50 of 132 micrograms protein/mL, but failed to suppress LBRM proliferation below 50% of control. CONCLUSION: These results suggest that the BeWo cell line is a promising model for the study of trophoblast-derived suppressive factors and that these factors can be generated in serum-free medium.

Animals↗
PubMed1994

Immunosuppression by hydatidiform mole trophoblast is neutralized by monoclonal antibodies to beta-interferon.

PROBLEM: In sheep and cattle, trophoblast-derived interferons serve as signals for the maternal recognition of pregnancy and may regulate the immunologic relationship between the fetus and mother. METHOD: In this study, soluble extracts prepared from human hydatidiform mole decidua (DE) and trophoblast (HME) were screened for immunosuppressive activity using an interleukin (IL)-2-dependent T-cell line (CTLL2). Antibody neutralization studies were performed with monoclonal antibodies to alpha- and beta-interferon (IFN). RESULTS: HME suppressed (P < 0.05) IL-2-stimulated (2 IU/well) CTLL2 proliferation at doses ranging from 500 (52 +/- 2% of control) to 100 (74 +/- 5%) micrograms/ml concentrations. DE also suppressed (P < or = 0.05) CTLL2 proliferation in a dose-related fashion from 500 (20 +/- 6% of control) to 100 (71 +/- 8%) micrograms/ml doses. Preincubation with the alpha- and beta-IFN antibody preparations had no effect on CTLL2 suppression by the DE sample. In contrast, the beta-IFN antibody partially neutralized the suppressive activity of HME at each of the dilutions tested. The monoclonal antibody to alpha-IFN failed to neutralize HME suppression at any of the doses tested. CONCLUSIONS: These results suggest that hydatidiform mole trophoblast produces a beta-IFN-like macromolecule that may abrogate maternal rejection responses that are harmful to the developing fetal allograft.

Antibodies, Monoclonal↗
PubMed1994

Gestational age correlates with immunosuppressive properties of hydatidiform mole pregnancies.

PROBLEM: Soluble trophoblast extracts (HME) from some human hydatidiform mole pregnancies suppress IL-2-dependent T-cell proliferation, while others express no immunosuppressive bioactivity. This study was designed to determine if suppression by HME was correlated with gestational age, uterine size, or hCG secretion. METHOD: Soluble extracts were prepared from nine hydatidiform mole trophoblast samples and screened for immunosuppressive activity using a murine cytotoxic T-cell proliferation assay (CTLL-2). Gestational ages were determined from last menstrual cycle and uterine size was estimated at the time of surgery. Serum samples were collected prior to uterine evacuation and were assayed for human chorionic gonadotropin (hCG). RESULTS: Four of nine HME samples significantly (P < 0.05) suppressed CTLL2 proliferation, while five exhibited no suppressive activity. A strong positive correlation (r = 0.639) was noted for the relationship between gestational age of the molar pregnancies and interleukin-2 (IL-2)-stimulated CTLL2 proliferation (expressed as % of control) in the presence of HME (500 micrograms/mL). This indicates that HME suppression of CTLL2 proliferation is highest in early gestation and then declines with increasing gestational age. A similar correlation was observed between estimated uterine size at surgery and CTLL2 proliferation with added HME, although the association was not as strong (r = 0.359). No association was noted between hCG levels and CTLL2 proliferative responses (r = -0.091). CONCLUSIONS: The results of this study suggest that production of immunosuppressive factors by hydatidiform mole trophoblast is developmentally regulated, and decreases with advancing gestation.

Cells, Cultured↗