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Biomedical subjects

I Berczi

Publications and source records attributed to I Berczi.

At least 73 records · Page 4Linked to original sources
PubMed1980

Antigen(s) expressed on cultured cells of various species that crossreact with tumor antigens(s).

Antibodies eluted from a methycholanthrene induced sarcoma (MC-D) of strain 13 guinea pigs were examined for reactivity against 11 cultured cell lines derived from unrelated tumors and 11 cell lines originating from normal tissues of various species by radioimmunoassay. Six tumor-derived lines of mouse, hamster, rat, guinea pig and man and five "normal" cell lines of guinea pig, human and fish origin showed significant reaction.

Animals↗
PubMed1979

Detection of tumor antibodies in patients with gastrointestinal carcinomas by a solid-phase radioimmunoassay.

Metastatic tumors from livers of 5 patients with gastrointestinal carcinomas and from the liver of 1 patient with malignant breast carcinoma were extracted with 3 M KCl; similar extracts were prepared from normal human colon and liver and from human fetal gut. The extracts were depleted of serum globulins by passage through reverse immunoadsorbent columns consisting of rabbit antibodies to the F(ab)2 fragment of human IgG and were then coupled to CNBr-activated paper disks. These "antigen" disks were used in a radioimmunoassay, with the aid of 125I-labeled rabbit antihuman F(ab')2 antibodies for the assay of circulating tumor antibodies produced by cancer patients. Statistical evaluation of the results with plasma samples from 47 patients with colorectal carcinomas and from 7 patients with other gastrointestinal disorders (polyps, villous papilloma, diverticulitis, and Crohn's disease) indicated that a significant number of patients had antibodies to cross-reactive tumor antigen(s). The cross-reactive tumor antigen(s) involved in the reaction was not detected in extracts of the gastrointestinal tract from 12-week human fetuses and did not cross-react with carcinoembryonic antigen.

Adult↗
PubMed1979

Rejection of tumor cells in vitro: morphological studies on killer T cells and damaged tumor cells.

The in vitro destruction of a methylcholanthrene-induced guinea pig sarcoma (MC-D) by killer T lymphocytes was investigated by light and electron microscopy. Various degrees of cell damage ranging from slight to extensive were observed. In cells with slight injury, dilatation, vesiculation, fragmentation and degeneration of the rough surfaced endoplasmic reticulum were the most characteristic findings. In cells with extensive injury, widespread nuclear and cytoplasmic alterations were evident and many of these cells were fragmented into smaller portions and finally transformed into granular membranous and amorphous debris. Cytoplasmic vacuoles filled with electron-lucent material were frequent in extensively damaged cells. Killer lymphocytes resembled closely antibody-forming plasma cells when examined with light microscopy but lacked the extensive network of rough surfaced endoplasmic reticulum, and did not produce immunoglobulin. It is suggested that these extensively differentiated T-derived killer cells are end cells similar to those of B lymphocyte-derived plasma cells. Viral particles resembling closely C-type viruses were observed in mixed killer cell MC-D cultures.

Animals↗
PubMed1978

Immunodeficiency in hypophysectomized rats.

The response of hypophysectomized, sham-operated and non-operated female Fischer 344 and Wistar-Furth rats was compared to various antigenic stimuli. Antibody production against sheep red blood cells, skin response to dinitrochlorobenzene and the development of adjuvant arthritis after treatment with Freund's complete adjuvant were all markedly suppressed in hypophysectomized animals. Sham-operated rats responded as well as did non-operated controls. Skin graft survival was also prolonged in hypophysectomized rats when compared to controls. These results indicate that the pituitary gland plays an important role in immune reactions.

Animals↗
PubMed1977

Resistance of guinea-pig hepatoma cells to complement-mediated lysis induced by ascites fluid or serum from tumor-bearing animals.

The mechanisms of tumor cell susceptibility and resistance to cytotoxic antibodies were investigated in the guinea-pig ascites hepatoma (line-1 and line-10) system. Treatment of line-specific rabbit antibody-coated tumor cells by ascitic fluid, by serum of tumor bearers or by tumor extract inhibited subsequent complement-mediated lysis. Inhibition by ascitic fluid and serum was not line-specific, but inhibition by tumor extract was line-specific. Treatment of tumor cells with ascitic fluid or tumor extract prior to exposure to specific cytotoxic antibody and complement did not inhibit lysis. Incubation of cytotoxic rabbit antisera with ascitic fluid, tumor-bearer serum or tumor extract neutralized their complement-dependent cytotoxic activity on tumor cells. Tumor-immune guinea-pigs exhibited line-specific delayed cutaneous reactions after injection with ascitic fluid or tumor extract. Studies with indrect immunofluorescence revealed that exposure to ascites fluid or tumor extract caused a rapid shedding of rabbit antibodies from the tumor cell surface. Evidence is presented indicating that the active fraction of ascites fluid was associated with immune complexes consisting of IgG and tumor antigen in excess. The relevance of these findings to tumor escape from immune destruction in vivo is discussed.

Animals↗
PubMed1977

Susceptibility to and escape from complement-mediated lysis of guinea-pig hepatoma line-10.

Rabbit xenoantisera produced against diethyl-nitrosamine-induced strain-2 guinea-pig hepatoma line-10 cells (L-10) according to various immunization schedules were compared for their cytotoxicity on L-10 cells in the presence of guinea-pig complement. The highest activity was obtained with antisera (Cx-1) produced by repeated intravenous injections of living L-10 cells at high cell dosage, whereas intramuscular injections of living or glutaraldehyde-treated L-10 cells at similar frequency and cell dosage were less effective for the production of cytotoxic antibodies against L-10 cells. Intravenous injections of smaller cell doses were less effective. The cytotoxic antibody in Cx-1 antiserum was shown to be IgG by various methods including gel filtration on Sephadex G-200, ion exchange chromatography and immunoelectrophoresis of purified tumor-specific antibodies. It was concluded that L-10 cells can be lysed by guinea-pig complement and tumor-specific antibodies (IgG). Some antisera contained IgM antibodies which were not cytotoxic. A decrease in susceptibility of L-10 cells to complement-mediated lysis was observed when the cells were maintained in vivo for a long period (more than 20 passage generations). This was due to a lower density of tumor antigens on the cell surface. When tumor cells were treated with a second antibody directed against rabbit IgG or F(ab')2, cytotoxicity of Cx-1 antisera was completely abolished.

Animals↗
PubMed1977

Tumor inhibition by effector cells cultured from progressing sarcomas.

The effect of cytotoxic lymphoid cells emerging in primary cultures of an antigenic sarcoma of strain 13 guinea pigs was investigated on tumor growth in vivo. The growth of lethal tumor inocula was inhibited or the tumor cells were completely rejected in normal syngeneic recipients treated s.c. with low doses (5 X 10(5)) of effector cells which were mixed with the tumor cells. A higher dose (2.5 X 10(6)) of killer cells did not affect significantly tumor growth in normal recipients. Significant tumor inhibition was observed in X-irradiated recipients given high doses (2.2 X 10(6)) of effector cells locally although rejection did not occur with high frequency. Local treatment of X-irradiated recipients with low doses (5 X 10(5)) of effector cells did not influence tumor growth. Systemic treatment of normal or X-irradiated recipients with effector cells had little effect at any dose, although tumor inocula were occasionally rejected. Sonication of the cytotoxic effector cells prior to administration inhibited their tumor suppressing effect. Animals that rejected the first tumor inoculum were immune to a second lethal dose of sarcoma cells. It is indicated by the results that tumor rejection in vivo is not simply a matter of killer-target cell interaction, but rather a complex and poorly understood phenomenon.

Animals↗
PubMed1976

Efferent enhancement of a methylcholanthrene-induced sarcoma transplantable in strain 13 guinea pigs.

The immunobiology of an antigenic methylcholanthrene-induced sarcoma (MC-D) of inbred strain 13 guinea pigs has been investigated. The induction of concomitant immunity by growing MC-D tumors was indicated by the suppression of small tumor inocula in the presence of a large tumor cell dose and by the regression of intradermal tumor nodules. Furthermore, it was demonstrated that this tumor was coated with antibody in vivo. Previous studies showed that MC-D tumors were infiltrated with killer T cells which were capable of complete tumor destruction in vitro, but could never induce spontaneous regression in vivo. On the basis of all these facts, antibody-mediated efferent enhancement is proposed to be the major escape mechanism of this tumor.

Animals↗
PubMed1975

Rejection of tumor cells in vitro: a T-cell-mediated reaction.

Cytoxic lymphoblasts (LBC) were produced by the co-cultivation of guinea-pig lymphoid cells from the thymus, lymph nodes, spleen, bone marrow and blood with syngeneic methylcholanthrene-induced sarcoma (MC-D) cells. The cytotoxic reaction was inhibited by pretreatment of the lymphoid cell populations with a rabbit antiserum specific for guinea-pig thymus-derived (T) lymphocytes. Supernatants of LBC inhibited the migration of peritoneal exudate cells, but did not contain lymphotoxin or a skin reactive factor. It is concluded that the cytotoxic cells are of T-cell origin.

Animals↗
PubMed1975

A microradioimmunoassay for antibodies to tumor-associated antigens.

A versatile microradioimmunoassay for the detection of antibodies to tumor-associated and other tissue antigens was described. The method involved: a) the preparation of solid-phase antigen with cultured (already adhered) or noncultured cells (sedimented by centrifugation) fixed to Micro-Test plates with neutral buffered formaldehyde or absolute methanol; b) the incubation of the antigen with test or control sera; and c) the incubation of the antigen with radioiodinated antiglobulin antibody. The nonspecific background of radioactivity was reduced to an acceptable level by the fixed cells being precoated in the wells with 0.5% bovine serum albumin in phosphate-buffered saline which was also used for the dilution of sera and labeled antiglobulin antibody. Tumor cells in primary cultures gave a high background, as compared to long-term cultures, which was due to the presence of immunoglobulins (most likely tumor-specific antibody). The specific antibody response to a syngeneic mouse tumor was demonstrated by this technique.

Animals↗
PubMed1973

Rejection of tumor cells in vitro.

The emergence of lymphoblast-like cells, capable of rapidly destroying tumor cells, was observed in primary cultures of an antigenic sarcoma transplantable in strain 13 guinea pigs. It is likely that these cytotoxic cells represent the progeny of lymphocytes sensitive to tutmor antigens that had infiltrated the tumor tissue.

Animals↗