Studies on T-Lineage Cells in Human Decidua of First Trimester Pregnancies

ABSTRACT: T-lineage cells in human decidua of early pregnancies were tested for surface markers, proliferative response, interleukin-2 (IL-2) production, and natural killer (NK) activity. T-lineage (CD2⁺) cells that were obtained from decidua by the use of E-rosette formation contained fewer CD3⁺ mature T cells and CD4⁺ cells than those from the peripheral blood of the same donors, while no differences were seen in the frequencies of CD8⁺ cells. P55 molecules of IL-2 receptor (IL-2R/p55, Tac antigen) were hardly detected on fresh decidual T-lineage cells, though approximately 20% were positive for HLA-DR. More than a half of decidual T-lineage cells expressed CD56 molecules on their surface and killed K562 cells, the prototype target of NK cells, while most of them were negative for CD16 and CD57. Upon stimulation with IL-2, decidual T-lineage cells demonstrated dose-dependent proliferative response. In addition, they were induced to produce high amounts of IL-2 by stimulation with mitogens but not with alloantigens. These results suggest that human decidua contains high numbers of CD2⁺3-CD16⁺56⁺ lymphocytes and that this population responds to IL-2, produces IL-2 and mediates NK activity.     

Suppression by Human Placental Protein 14 of Natural Killer Cell Activity

ABSTRACT: Human decidua of early pregnancy contains considerable numbers of CD3^? CD56⁺ natural killer (NK) cells. In this study, two major protein products of the decidua, placental protein 14 (PP14) and placental protein 12 (PP12), were tested for the ability to regulate human NK cell activity. In vitro overnight exposure to PP14 of blood lymphocytes or purified large granular lymphocytes (LGL) resulted in suppression of cytotoxicity against K562 target cells in a 4-h ⁵¹Cr release assay. The NK inhibition was dependent on concentrations of PP14, being detectable at 5 μg/ml and reaching maximum at 50 μg/ml. Manifestation of PP14-induced NK suppression required 18-h contact with NK cells. The suppression of NK activity by PP14 was not abolished by indomethacin. In a target binding assay the number of PP14-treated LGL binding to K562 was comparable to that of untreated ones. By contrast with PP14, PP12 produced no effects on NK cells. These results indicate that PP14 suppresses the function of NK cells, which might be involved in prevention of maternal immune rejection of fetus at the fetomaternal interface.     

Defects in the precore region of hepatitis B virus DNA in a plasma pool from carriers seropositive for antibody against e antigen and with infectivity in chimpanzees

A plasma pool from 12 asymptomatic carriers seropositive for antibody against hepatitis B e antigen (anti-HBe) contained hepatitis B virus (HBV) with chimpanzee infectious doses of 1-100/mL, and another pool from 12 carriers positive for hepatitis B e antigen (HBeAg) contained 10(8)/mL doses or more. The HBeAg-positive pool contained 10(6)-fold more HBV DNA than the anti-HBe-positive pool, reflecting the difference in infectivity in chimpanzees. The precore region sequences of HBV DNA in the two plasma pools were amplified by polymerase chain reaction, and separate HBV DNA clones were propagated for determining the nucleotide sequence. Of 114 clones from the anti-HBe-positive pool, 113 displayed a point mutation from guanine to adenine at nucleotide 83 in the precore region, which converted codon 28 for tryptophan (TGG) to a stop codon (TAG), and the remaining clone had a point mutation from adenine to cytosine at the first letter of codon 1 (CTG) to inhibit the translation initiation of the precore region. Precore region defects, in contrast, were observed in only 10 (8%) of 119 clones from the HBeAg-positive pool. These results indicate the infectious capacity of HBV mutants, defective in the precore region and incapable of directing the synthesis and secretion of HBeAg, which prevail in the circulation of hosts after they seroconvert from HBeAg to anti-HBe.     

Retrograde Multiple and Multifiber Accessory Pathway Conduction in the Wolff-Parkinson-White Syndrome:

Retrograde Multiple Accessory Pathway Precipitating AF. Introduction : The determinants of susceptibility to atrial fibrillation (AF) and the existence of accessory pathway conduction have remained unidentified in the Wolff-Parkinson-White (WPW) syndrome. We tested the hypothesis that excitation inputs into the atrium over a retrograde multiple or multifiber accessory pathway during AV reentrant tachycardia (AVRT) could precipitate initiation of AF.
Methods and Results : Two hundred fifty consecutive patients with WPW syndrome underwent electrophysiologic study and radiofrequency catheter ablation. The patients were classified into two groups according to the study results: 29 with retrograde multiple or multifiber accessory pathway (MP) and 221 with retrograde single accessory pathway (SP). Compared with the SP patients, the MP patients showed a significantly higher incidence of clinical AF (MP vs SP: 19/29 vs 51/221, P < 0.01), induced AF (12/29 vs 32/221, P < 0.01), and initiated AF during ventricular pacing and AVRT (10/12 vs 17/32, P < 0.05). There were no differences between the two groups in incidence of clinical and induced AVRT (24/29 vs 200/221 and 25/29 vs 206/221, respectively), mean cycle length of induced AVRT, or electrophysiologic parameters of the accessory pathway. AF inducibility during AVRT or ventricular pacing was eliminated by partial ablation in 7 of 10 patients with MP. After total ablation, the incidence of induced AF was similar between the two groups (MP vs SP: 1/29 vs 11/221).
Conclusion : The existence of a retrograde multiple or multifiber accessory pathway in patients with WPW syndrome is associated with a higher incidence of clinical and induced AF. Successful ablation of the retrograde multiple or multifiber accessory pathway can eliminate the induction of both AVRT and AF.