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Biomedical subjects

I D Bernstein

Publications and source records attributed to I D Bernstein.

At least 145 records · Page 8Linked to original sources
PubMed1980

T cell synergy in the rat: serologic characterization of T cell subsets.

The W3/25+ T cell subset in rats, defined by a xenogeneic monoclonal antibody and separated by using the FACS, was demonstrated to be the proliferating cell type in the in vitro MLC and to provide an amplifier function for the W3/25- T cell subset in the generation of cytotoxic effector cells to alloantigenic targets.

Animals↗
PubMed1979

Cell-mediated reactivity to antigens shared by Moloney-virus-induced lymphomas (LSTRA) and certain 3-methylcholanthrene-induced mouse sarcomas.

Spleen cells (SC) both from BALB/c mice whose primary Moloney sarcoma virus (MSV)-induced sarcomas had spontaneously regressed and from normal, untreated BALB/c mice, were co-cultivated for 5 days with mitomycin-C-treated LSTRA cells; LSTRA is a BALB/c Moloney lymphoma which shares cell surface antigens with MSV-indiced sarcomas. These SC, referred to as CMR and CU cells, respectively, were shown to be cytotoxic to LSTRA cells in 3 h 51Cr-release assays; CMR cells showed, in most cases, the greatest lytic activity against LSTRA targets. The same SC were also reactive, in 20-h microcytotoxicity and 51Crassays, against target cells from a variety of transplanted sarcomas indiced by 3-methylcholanthrene (MCA) in Balb/c mice. The highest reactivity was seen when CMR or CU cells were tested against target cells from sarcoma lines that expressed an NB-ecotropic MuLV cross-reacting serologically with Moloney virus. Reactivity against isotope-labelled tumor cells expressing MuLV-associated cell surface antigens could be competititively inhibited by adding unlabelled tumor cells expressing such antigens. Finally, Winn assays were performed in which CMR cells strongly inhibited the outgrowth of cells from three sarcoma lines that express the NB-ecotropic MuLV. There was less but significant inhibition of cells from some other MCA sarcomas, either negative for the expression of MuLV-associated antigens or expressing the N-ecotropic endogenous BALB/c MuLV. CU cells enhanced tumor outgrowth in Winn assays at least as often as they inhibited it.

Animals↗
PubMed1979

Improved remission induction rate with D-ZAPO but unimproved remission duration with addition of immunotherapy to chemotherapy in previously untreated children with ANLL.

In 163 children with acute nonlymphocytic leukemia (ANLL), a D-ZAPO induction program consisting of daunomycin, 5-azacytidine, cytosine arabinoside, prednisone, and vincristine resulted in a remission rate of 71.8%. Immunologic therapy was employed during maintenance with the aim of prolonging remission and improving survival. The administration of immunotherapy consisting of a mixture of bacillus Calmette-Guérin (BCG) and allogenic acute myelomonocytic leukemic cells injected intradermally on day 14 of each of the first three monthly cycles of 6-thioguanine for ten days, 5-azacytidine and cytosine arabinoside for four days, and vincristine for one day did not improve remission duration or survival compared to that due to chemotherapy alone. Important prognostic factors identified in this study included a remission induction rate significantly better for females than males (P = 0.04), for children between the ages of 5 and 10 years compared to those greater than this age group (P = 0.01), and a prolonged remission duration (P = 0.04), and survival (P less than 0.01) for patients with initial white blood counts of less than 20 x 10(9)/liter.

Adolescent↗
PubMed1979

Tumor-enhancing suppressor activator T cells in spleens and thymuses of tumor immune mice.

Cells from the spleens and thymuses of BALB/c mice whose Moloney sarcoma virus (MSV)-induced, primary sarcomas have regressed 2-3 months earlier ("MSV regressors") or are in the process of regressing can, when adoptively transferred to syngeneic mice given MSV at the age of 20 days, prevent the natural regression of the MSV sarcomas in the recipient mice. The cells responsible for this tumor-enhancing effect express the Thy 1 marker. They are not demonstrable in the thymuses of normal untreated mice or in mice that have either been immunized against or are bearing methylcholanthrene-induced sarcomas. The tumor-enhancing cells are not destroyed after administration of 400 rads (1 rad = 1.00 x 10(-2) J/kg) of whole body radiation. However, the effect of the irradiated cells is seen only in the presence of a nonirradiated T-cell population, represented in the thymuses of normal control mice, with which we postulate that they interact. Studies on a transplantable, chemically induced, murine leukemia virus antigen-negative sarcoma, MCA-1460, further support the concept that relatively radioresistant thymus cells from immune mice can enhance tumor outgrowth by interacting with radiosensitive T cells that are present in nonimmune mice.

Animals↗
PubMed1978

Granulopoietic increase by BCG in mice.

Repeated doses of the non-specific immunostimulant BCG were injected intraperitoneally, followed by serial measurement of serum colony stimulating factor (CSF), and CFU-C number and percent synthesizing DNA. Following primary challenge with BCG, CSF remained at low levels until day 7, rose to a peak by day 10, and remained elevated through 14 days. Secondary challenge resulted in a bi-phasic CSF response with a small peak on day 1 and a larger one by day 7. Following secondary challenge, the percent of CFU-C in 'S' phase doubled in 24 hours; CFU-C significantly increased in number by 48 hours. The studies suggest that the marrow toxicity of cycle active cytotoxic drugs might be altered by non-specific immunostimulants such as BCG.

Animals↗
PubMed1978

Phase II study of the failure of vincristine and bleomycin for previously treated children with metastatic neuroblastoma: a report from the Childrens Cancer Study Group.

Twenty-two patients with previously treated but progressive stage IV neuroblastoma received combination therapy with vincristine (1.0 mg/m2) followed in 6 hours by bleomycin (15 mg/m2). Therapy was administered twice weekly. No responses were seen in the 19 patients who received four or more doses of the bleomycin-vincristine combination.

Bleomycin↗
PubMed1977

In vitro reactivity in allograft tolerance: persistence of mixed leukocyte culture reactivity in highly tolerant rats.

Mixed leukocyte culture reactivity was studied in adult W/Fu rats judged to be highly tolerant after the inoculation of (W/Fu X BN)F1 hybrid spleen and bone marrow cells at birth. Reactivity was observed in a majority of tolerant donors tested and documented by quantitative dose-response and kinetic studies. Allograft tolerance cannot be explained by a complete lack of specific immune reactivity to tolerated alloantigens.

Animals↗
PubMed1977

Passive transfer of systemic tumor immunity with cells generated in vitro by a secondary immune response to a syngeneic rat gross virus-induced lymphoma.

Spleen cells taken from W/Fu rats 4 to 6 weeks after immunization with the syngeneic Gross virus-induced lymphoma, (C58NT)D cells, at a time when they lack detectable activity in a short-term 51Cr release assay, were previously shown to retain the capacity to generate cytotoxic activity upon reexposure to mitomycin C-treated lymphoma (C58NT)D cells in vitro. In the studies presented here, we evaluated whether in vitro sensitization of immune lymphoid cells before systemic transfer to a nonimmune recipient allows for more effective transfer of tumor immunity. The results show that the passive transfer of immune spleen cells after in vitro cocultivation with mitomycin-treated (C58NT)D cells allows for inhibition of growth of a subcutaneous inoculum of lymphoma cells. In contrast, spleen cells obtained 4 to 6 weeks after primary sensitization or after secondary in vivo sensitization did not effectively confer anti-tumor immunity. As few as 5 x 107 in vitro sensitized cells permitted complete inhibition of 106 (C58NT)D cells and also allowed for inhibition of the growth of 107 (C58NT)D-F cells, which was lethal to control animals. Immune cells sensitized with syngeneic thymocytes or normal spleen cells sensitized with (C58NT)D cells in vitro did not confer in vivo anti-tumor immunity. After systemic transfer of in vitro sensitized cells, delayed hypersensitivity occurred at the site of tumor inoculation and tumor growth was suppressed. Specificity of the passive immunity was shown by the failure to inhibit growth of a polyoma virus-induced sarcoma in rats which inhibited growth of the Gross virus-induced lymphoma cells. In vitro sensitized cells were more effective in the transfer of anti-tumor protection after 5 days, as compared to 2 days, of cocultivation with tumor. Results show that in vitro sensitized cells can effectively transfer systemic tumor immunity.

AKR murine leukemia virus↗
PubMed1977

Relationship of cellular proliferation and the generation of cytotoxic cells in an in vitro secondary immune response to syngeneic rat lymphoma cells.

The role of cellular proliferation for the generation of cytotoxic activity in an in vitro secondary immune response to syngeneic lymphoma cells was investigated. Spleen cells from W/Fu rats immunized with the syngeneic (C58NT)D tumor proliferate and generate cytotoxic potential for tumor targets after exposure to mitomycin C-treated (C58NT)D cells in vitro. Elimination of proliferating cells by exposure to high specific activity 3H thymidine at approximate intervals impaired the generation of cytotoxic activity. Elimination of cells proliferating to either syngeneic lymphoma or BN rat alloantigens allowed the remaining cells to generate cytotoxic potential to the second set of antigens. Elimination of proliferating cells also abrogated the ability of the in vitro generated cells to adoptively confer anti-tumor protection on nonimmune recipients. These results demonstrate that cellular division is required for the generation of cells which are cytotoxic in vitro and can adoptively confer anti-tumor protection in vivo.

Animals↗