Clinical studies on cell-mediated immunity in gestational trophoblastic disease: nonspecific cellular immunocompetence in patients with hydatid mole and trophoblastic neoplasia.
The nonspecific cell-mediated immunocompetence of 51 patients with gestational trophoblastic disease (GTD), including 16 patients with hydatid mole (HM), 24 with nonmetastatic trophoblastic neoplasia (NTN) and 15 with metastatic TN (MTN), was studied with the use of both in vitro and in vivo parameters of cell-mediated immunity (CMI) such as lymphocyte blastogenic response to phytohemagglutinin (PHA), subpopulation constitution, and delayed cutaneous hypersensitivity responses to 2,4-dinitrochlorobenzene (DNCB) and to purified protein derivative of tuberculin (PPD). The pretreatment cell-mediated immune status of patients with HM developing no malignant sequelae was shown to be essentially similar, in terms of both in vitro PHA and in vivo DNCB reactivities, to that of normal women and of patients with benign gynecological diseases. In patients with TN, however, there was a significant depression in the blastogenic lymphocyte response to PHA before evacuation of the mole, which was persistently demonstrated after uterine evacuation and more marked throughout the course of disease in patients with MTN, than in those with NTN, with a tendency to return to normal in remission. Moreover, patients with TN had a significant depletion of T lymphocytes as determined by rosette-forming cell procedures before treatment, which was most evident in patients with MTN. Plasma from the MTN patients was also shown to have an inhibitory effect on PHA responsiveness of lymphocytes from normal women. There was an increased incidence of impaired reactivity to DNCB in patients with TN (higher in MTN than in NTN), compared with HM and benign diseases, while no such difference in incidence was observed in response to PPD. On the basis of these findings, a preliminary characterization of altered immunocompetence in patients with TN and its mechanism are discussed.
D000328:Adult; D001386:Azides / Q000494:pharmacology; D001402:B-Lymphocytes / Q000032:analysis; D004247:DNA / Q000096:biosynthesis; D004137:Dinitrochlorobenzene / Q000494:pharmacology; D004342:Drug Hypersensitivity; D005260:Female; D006801:Humans; D006828:Hydatidiform Mole / Q000276:immunology* / Q000601:surgery; D006968:Hypersensitivity, Delayed / Q000139:chemically induced*; D007111:Immunity, Cellular; D008214:Lymphocytes / Q000378:metabolism; D009362:Neoplasm Metastasis; D010835:Phytohemagglutinins / Q000097:blood / Q000494:pharmacology; D011247:Pregnancy; D013601:T-Lymphocytes / Q000032:analysis; D014328:Trophoblastic Neoplasms / Q000276:immunology* / Q000556:secondary*; D014594:Uterine Neoplasms / Q000276:immunology* / Q000556:secondary*
D001386:Azides; D004137:Dinitrochlorobenzene; D010835:Phytohemagglutinins; C028784:phytohemagglutinin-P; D004247:DNA