摘要:

AbstractBlastogenic transformation of murine spleen cells elicited with concanavalin A was suppressed by serotonin 10−-12to 10−-6M, and marginally stimulated by its antagonists ketanserin and propranolol in low concentrations (10−-15to 10−-11M). Ketanserin (5-HT2receptor ligand) and propranolol (5-HT1Aand beta-adrenergic ligand) did not block the suppressive effect of serotonin if used along with it in equimolar concentrations (10−-9M). Ergot-alkaloid dihydroergosine suppressed, whereas dihydroergotoxin stimulated the bldstogenic transformation. Opposite effects of the agents were obtained in experiments with mouse myeloma X63/Ag 8.653 and hybridoma SHV 125 cell lines, which unlike normal lymphoid cells, are homologous cell populations and proliferate spontaneously. The data indicate that serotonin and its antagonists interfere directly with mitosis and/or autocrine stimulation of target cells.

ISSN:0892-3973    

DOI:10.3109/08923979509052726

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

AbstractSex hormones affect (auto)immune responses in various ways. Investigations of the effects of estrogens have produced contradictory results.We studied the effects of gender, gonadectomy and of (supra)physiological doses of (the orally active) ethinylestradiol (EE) in two spontaneous autoimmune disease models: the NZB/NZW F1 and NOD mice. In both models we confirmed the female preponderance and the aggrevating effects of gonadectomy in males but not in females.The accelerated mortality found in NZB/W mice treated with supraphysiological doses of EE was not associated with increased proteinuria, increased IgG-type anti-DNA levels or increased mononuclear cell infiltrations in the submandibular gland. In contrast, we found a severe reduction in body weight and in the weights of various organs (indications of toxicity), and a decrease rather than an increase in proteinuria and in mononuclear cell infiltrations (indications for autoimmunity). Physiological doses of EE did not significantly affect disease symptoms.In the NOD model a near-physiological, non-toxic dose of EE did not cause consistent changes on immunological disease symptoms either.Therefore, we conclude that the sexual dichotomy in spontaneous autoimmune models is due to protective effects of androgens and that the mortality by estrogens is due to toxic effects rather than accelerated autoimmunity.

ISSN:0892-3973    

DOI:10.3109/08923979509052727

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

AbstractThe effect of cells from the liver of C3H fetuses syngeneic to splenic responder cells on an allogeneic mixed lymphocyte response (MLR) was studied. After fractionation on ficoll-hypaque, interface cells from corn oil (vehicle for BP) or normal fetal liver (FL) controls (CO), obtained from 17–19 days gestation, enhanced proliferation in the mixed lymphocyte culture (>2-fold), while cells from FLs transplacentally exposed to benzo(a)pyrene (BP) showed a decreased capacity for augmentation (>2-fold less than CO). Unfractionated CO-FL cells at 0.5×106did not augment proliferation, but at 0.10×256enhancement with control FL cells was significantly higher than with BP-FL cells. Pelleted cells from BP- and CO-FLs were severely suppressive at the higher dose, while at 0.25×106proliferation was augmented with CO-FL cells, but not affected with BP-FL cells. At doses of 0.1×106or less, no effect was observed for either control or BP-FL cells. These data indicate that: a) FL cells syngeneic to responder cells of an allogenic mixed lymphocyte culture (MLC) have an augmenting but not suppressive capacity on cell proliferation; b) in utero insult with BP modifies the capacity of FL cells to augment proliferation in the MLC.

ISSN:0892-3973    

DOI:10.3109/08923979509052728

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor

摘要:

AbstractHalothane hepatitis appears to result from an inappropriate immune response to the products of halothane metabolism. Attempts to produce an animal model for halothane hepatitis have been largely unsuccessful. Although guinea pigs produce neoantigens following treatment with halothane, the subsequent antibody response is weak, possibly accounting for the failure to produce halothane hepatitis in these animals. In order to increase the antibody response to halothane neoantigens, three methods for trifluoroacetylating proteins were used. Guinea pigs were either treated with S-ethylthiotrifluoroacetate, autologous lymphocytes trifluoroacetylatedex vivo, or immunized with trifluoroacetylated mycobacterial protein, followed by exposure to halothane, and examined for anti-halothane metabolite antibodies (anti-TFA antibodies). Animals treated with S-ethylthiotrifluoroacetate developed anti-TFA antibodies, and following exposure to halothane exhibited an enhanced antibody response. Treatment with trifluoroacetylated lymphocytes also resulted in an enhanced anti-TFA antibody response following halothane exposure. Immunization with trifluoroacetylated mycobacterial proteins resulted in very high anti-TFA antibody titers. However, subsequent exposure to halothane had no observable effect on specific antibody titers. Exposure to halothane, regardless of treatment, resulted in the production of anti-microsomal protein antibodies. Signs of halothane hepatitis were not observed, indicating that enhancement of the humoral immune response does not appear to be sufficient for production of halothane hepatitis.

ISSN:0892-3973    

DOI:10.3109/08923979509052729

出版商:Taylor&Francis    

年代:1995

数据来源: Taylor