Search PubMed⌕ Search

Biomedical subjects

I Berczi

Publications and source records attributed to I Berczi.

At least 55 records · Page 3Linked to original sources
PubMed1986

Effects of mycoplasma infection on Fc receptors for IgE of rat basophilic leukemia cells.

Earlier studies from this laboratory had shown that rat basophilic leukemia cells carry two major receptors for IgE, named R and H, and a third minor receptor, designated 71K. It is now apparent that 71K is induced by the action of Mycoplasma hyorhinis, a common contaminant of tissue cultures. This induction is reversible. Decontamination either in in vitro or in vivo leads to a disappearance of 71K and re-infection causes its reappearance. The 71K receptor appears to be induced by the action of the mycoplasma on a surface molecule, most likely R, present on the cells at the time of infection. When receptors are occupied by IgE, 71K induction is inhibited. Other effects of mycoplasma infection include the significant reduction in the expression of transferrin receptors and increased histamine content of infected cells.

Animals↗
PubMed1986

Immunomodulation by tamoxifen and pergolide.

Treatment of rats with tamoxifen citrate or pergolide mesylate was as effective in inhibiting antibody formation and contact sensitivity skin reactions as was hypophysectomy. The immunocompetence of tamoxifen citrate- and pergolide mesylate-suppressed animals could be fully restored by additional treatment with prolactin or growth hormone.

Animals↗
PubMed1985

Immunomodulation in rats by transplantable anterior pituitary tumors.

The effect on the immune response of the MtT/W5 (W5), MtT/W10 (W10) tumors of Wistar-Furth rats and of MtT/F4 (F4) tumor transplantable in Fischer 344 rats was examined. Antibody response to sheep red blood cells and contact sensitivity reactions to dinitrochlorobenzene (DNCB) were used as immune parameters. In intact rats the W5 tumor suppressed the antibody response as much as did hypophysectomy (Hypox). The antibody response of Hypox rats was marginally improved by this tumor. Contact sensitivity was not suppressed in intact animals and the poor reactivity of Hypox rats was reconstituted to normal levels by W5. Treatment with bromocriptine (BRC) had no influence on tumor growth or on the immune reactivity of tumor-bearing hosts. The W10 tumor suppressed antibody formation, but not contact sensitivity in intact animals; the antibody and the DNCB response of Hypox animals was reconstituted partially, by this tumor. BRC treatment of tumor-bearing animals mimicked the effect of Hypox in this system. The F4 tumor suppressed antibody formation in intact rats and did not reconstitute the reactivity of Hypox rats. The DNCB response was not influenced by this tumor in intact animals and it was partially reconstituted in Hypox rats. Again, the reactivity of BRC-treated animals was similar to that of Hypox tumor-bearing animals. These results indicate that pituitary tumors may alter the immune reactivity of their hosts significantly.

Adenoma↗
PubMed1984

The influence of pituitary hormones on adjuvant arthritis.

Adjuvant arthritis was induced in female Fisher rats by injecting their right hind paw with 0.1 ml Freund's complete adjuvant. The development of adjuvant arthritis was inhibited by hypophysectomy and by daily treatment of intact animals with the dopaminergic agent bromocriptine. Adjuvant arthritis developed normally if hypophysectomized or bromocriptine-suppressed animals were treated with either prolactin or growth hormone. Additional treatment with adrenocorticotropic hormone inhibited this restoration. Treatment of hypophysectomized rats with follicle-stimulating hormone, luteinizing hormone, and thyroid-stimulating hormone had no effect. These results indicate that prolactin and/or growth hormone are necessary for the development of adjuvant arthritis, whereas adrenocorticotropic hormone has an inhibitory effect.

Adrenocorticotropic Hormone↗
PubMed1983

Tumor-reactive IgE antibodies in plasma of patients with gastrointestinal carcinomas.

A total of 208 plasma samples from 115 patients with gastrointestinal carcinomas and nine patients with other intestinal disease were examined for the presence of IgE tumor antibodies by a solid-phase radioimmunoassay. Approximately one-third of the patients gave significant reactions with gastrointestinal carcinoma extracts compared with normal tissue extracts. Absorption with tumor and normal tissue extracts, with type AB human red cells, and with CEA indicated tumor specificity in some of the samples so examined. None of the 50 serum samples tested from normal blood donors contained tumor-specific IgE. IgE tumor antibodies decreased or completely disappeared in the majority of patients 8-13 days after surgical treatment.

Antibodies, Neoplasm↗
PubMed1983

Immunomodulation by bromocriptine.

Treatment of rats with the dopaminergic ergot alkaloid bromocriptine (BRC) inhibited the following immune reactions: contact sensitivity skin reaction to dinitrochlorobenzene (DNCB); antibody formation to sheep red blood cells and to bacterial lipopolysaccharide; adjuvant arthritis; and experimental allergic encephalitis. Immunosuppressive doses of BRC (5 mg/kg) decreased the serum prolactin (PRL) levels from 84.8 +/- 15.9 ng/ml to 4.9 +/- 1.6 ng/ml. Further studies on DNCB contact sensitivity and on antibody formation revealed that the immunocompetence of BRC-suppressed animals could be restored by additional treatment with either prolactin (PRL) or growth hormone (GH). Treatment with adrenocorticotropic hormone antagonized the restoring effect of PRL and GH. These results suggest that BRC suppressed immunity by its inhibition of PRL, and possibly also by inhibition of GH secretion.

Animals↗
PubMed1983

Pituitary hormones and contact sensitivity in rats.

Hypophysectomized (Hypo-X) rats do not develop contact sensitivity to dinitrochlorobenzene (DNCB). Daily treatment with prolactin or growth hormone completely restores the DNCB-reactivity of Hypo-X animals. Treatment of such animals with ACTH, FSH, LH, TSH or HCG has no restoring potential. Treatment with ACTH in addition to prolactin or growth hormone antagonizes restoration of Hypo-X rats. These experiments indicate that the pituitary gland has the potential of regulating contact sensitivity.

Adrenocorticotropic Hormone↗
PubMed1983

Regulation of immunity in rats by lactogenic and growth hormones.

Antibody formation to sheep red blood cells and the development of contact dermatitis in response to dinitrochlorobenzene are impaired in hypophysectomized (Hypo-X) rats. Rat prolactin, rat growth hormone, bovine prolactin, bovine growth hormone, human placental lactogen and human growth hormone all restored the immunological competence of Hypo-X animals. The possible mechanism of action of these hormones on immune reactions is discussed.

Animals↗
PubMed1982

Tumour cell-antibody interactions. II. In vitro studies.

The interaction of L5178Y thymic lymphoma cells syngeneic to DBA/2 mice and of normal thymocytes with goat IgG antibodies was studied in vitro. Viable tumour and normal cells exerted a rapid, continuous and temperature-dependent destruction of antibody activity. Fractionation studies of culture supernatants from antibody-coated cells revealed that a significant portion of the antibody was completely degraded to amino acids. Tumour cells digested antibody more effectively than did normal lymphocytes. This observed degradation of antibody was most extensive at 37 degrees, significantly less at room temperature (23 degrees) and not detectable at 0 degrees. Undegraded antibody released from antibody-coated cells had also lost its antibody activity to a considerable extent. This was due to the formation of soluble antigen-antibody complexes, which was observed even at 0 degrees. Cells fixed with 10% formalin bound maximum amounts of antibody were incapable of digesting antibody even at 37 degrees and did not release immune complexes. These findings are of relevance to cancer immunodiagnosis and immunotherapy.

Animals↗
PubMed1982

Tumour cell-antibody interactions. I. In vivo experiments.

Goats were immunized with membrane fractions of the L5178Y tumour syngenic to DBA/2 mice. IgG fractions of this antiserum were made tumour specific by repeated in vitro and in vivo absorptions with normal cells and concentrated by adsorption to and elution from tumour cells. In vivo studies indicated that the accumulation of 125I-labelled antibody in tumour tissue could not be improved by extensive purification and concentration. The observed clearance rates of radioactivity from tumours and whole animals showed that the metabolism of antibodies was significantly accelerated in the presence of target cells. It is suggested that a rapid neutralization and degradation of antibody by the target tissue prevents its accumulation in tumour nodules.

Animals↗
PubMed1981

Five different adenomas derived from the rat adenohypophysis: immunocytochemical and ultrastructural study.

With the use of electron microscopic morphology and immunochemistry, 5 tumors were studied: a spontaneous prolactin-producing adenoma (LEP rats); an estrogen-induced intrasellar tumor (R-Amsterdam rats); and 3 transplanted tumors, MtT.W10 and MtT.W5 (WF rats) and MtT.F4 (F344 rats). All tumors were derived from rat adenohypophysis and are known to secrete prolactin, growth hormone, or adrenocorticotropic hormone. The spontaneous tumor consisted of a uniform population of cells containing only immunoreactive prolactin. In the estrogen-induced tumor, prolactin and growth hormone were localized in separate cell types with the use of the immunoperoxidase technique. In the MtT.W10 tumor, both immunoreactive prolactin and growth hormone were observed in the same cell and in separate cell types. In the MtT.F4 and MtT.W5 tumors, one cell type was identified that was characterized by lack of morphologic differentiation, reduced secretory granule number, and inconclusive immunopositivity.

Adenoma↗
PubMed1981

Prolactin and contact sensitivity.

Hypophysectomized (Hypo-X) rats did not develop contact dermatitis in response to dinitrochlorobenzene (DNCB). Syngeneic pituitary grafts placed under the kidney capsule or daily treatment with prolactin restored the DNCB-reactivity of Hypo-X animals. Combined treatment with other pituitary hormones was ineffective. Treatment of normal rats with a potent prolactin antagonist drug, bromocriptine, was as effective in inhibiting contact sensitivity as was hypophysectomy. These results indicate the contact sensitivity is a prolactin dependent reaction.

Animals↗
PubMed1981

Regulation of humoral immunity in rats by pituitary hormones.

Hypophysectomized female Fischer 344 and Wistar-Furth rats had severely impaired primary and secondary antibody responses to sheep red blood cells (SRBC). Mercaptoethanol-sensitive (IgM) and mercaptoethanol-resistant (IgG) antibodies were similarly affected. Titers to E. Coli 055:B5 lipopolysaccharide were also significantly decreased in such animals. The antibody response of hypophysectomized rats could be restored by syngeneic pituitary grafts when placed under the kidney capsule or by prolactin treatment. Growth hormone was less effective in this respect than prolactin. Treatment of normal rats with ACTH suppressed their antibody formation to SRBC. These results indicate that the pituitary gland has the potential to regulate humoral immune responses.

Adrenocorticotropic Hormone↗
PubMed1981

Human B lymphocytes activated by Epstein-Barr virus (EBV) or by mitogens suppress mitogen-induced immunoglobulin production.

Polyclonal activation of human B lymphocytes by LPS or protein A, alone or in combination or by Epstein-Barr virus (EBV), generates suppressive conditions that inhibit the response of human B lymphocytes to pokeweed mitogen (PWM), measured by the induction of immunoglobulin-secreting cells (PFC). Moreover, EBV-transformed B cell lines of normal or neoplastic (Burkitt lymphoma) origin also suppressed the PWM-induced immunoglobulin production of normal B cells. Cell separation experiments have shown that mitogen activated autologous B cells stimulate suppressor T cells in a similar way as B cell-derived lymphoblastoid cell lines. The significance of this phenomenon is considered in relation to the escape of the activating microorganism or virus from immune control and the occurrence of network interactions within the immune system.

Antibody-Producing Cells↗
PubMed1980

Effector and enhancing lymphoid cells in plasmacytoma-bearing mice. I. Methodological studies on the Winn assay.

Some parameters of the Winn assay for the detection of tumor-suppressing ("effector") and tumor-enhancing lymphoid cells were studied in BALB/c mice. Spleen cells of mice that were preimmunized with mitomycin-C-treated MOPC-104E plasmacytoma cells were inhibitory in this test system for both the MOPC-104E and the HOPC-I plasmacytomas, thus indicating cross-reactivity. Spleen cells taken from mice 6 days after the surgical removal of 15-day-old MOPC-104E tumors inhibited the growth of lethal doses of MOPC-104E cells in normal recipients, but no inhibition was observed 2 days after the removal of 18-day-old tumors. Spleen cells from mice bearing MOPC-104E for 13 days enhanced tumor growth. This enhancement was not influenced significantly by the wide dose range (from 10(5) to 3 x 10(7)) of MOPC-104E cells used to initiate tumors in the lymphoid cell donors, although tendency for stronger enhancing potential occurred after low tumor doses. When spleen cells from donors bearing MOPC-104E for 10 days were injected at the constant tumor-lymphocyte ratio of 1:30 with increasing numbers of tumor cells (from 5 x 10(5) to 2 x 10(6)), tumor inhibition occurred at the lowest dose only, while no significant effect was observed at higher tumor cell doses. When a constant dose (5 x 10(5)) of tumor cells was injected with spleen cells from 10-day tumor-bearers at tumor/lymphocyte ratios of 1:10, u:40 and 1:160, a significant tumor inhibition occurred only at the ratio of 1:40. The relevance of the Winn test to the study of immune mechanisms in tumor-bearing hosts is discussed.

Animals↗
PubMed1980

Effector and enhancing lymphoid cells in plasmacytoma-bearing mice. II. Dynamic changes during tumor progression.

The Winn assay was used for the study of effector (tumor-inhibiting) and enhancing (tumor-promoting) lymphoid cells in BALB/c mice bearing MOPC-104E plasmacytomas. Kinetic studies with thymus, lymphnode, spleen and bone-marrow cells revealed that spleen, lymph node and to a lesser extent bone-marrow cells from 7- and 10-day tumor-bearers inhibited MOPC-104E growth, while at day 13 all three cell populations enhanced tumor growth. However, at day 16 strong tumor inhibition was observed again by spleen cells and to a lesser extent by lymph-node cells and thymocytes. Peritoneal cells from normal and tumor-bearing (7 and 10 days) animals enhanced tumor growth significantly. Separation of spleen cells on nylon wool columns showed that at 10 days the effector cells were T lymphocytes, but at a later stage (35 days) a different effector mechanism was present in the spleen. Treatment of MOPC-104E recipients with carrageenan or silica had little influence on tumor growth, but marked tumor inhibition occurred after lethal irradiation and bone-marrow reconstitution. This latter observation, together with the finding that bone-marrow, lymph node and peritoneal cells from normal donors enhanced tumor growth in several experiments, suggests that this plasmacytoma, like hormone-dependent tumors, requires lymphocyte-derived growth factors.

Animals↗