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S Ben-Efraim

Publications and source records attributed to S Ben-Efraim.

141 records · Page 8Linked to original sources

Effect of mitogen-induced stimulation on DNase activity in lymphocytes.

The effect of mitogen-induced stimulation in spleen cells and thymocytes of BALB/c mice on acid DNase-activity levels was determined. Increase in thymidine uptake induced by either LPS or ConA in spleen cells and by ConA in thymocytes was invariably accompanied by parallel increase in acid DNase activity. Treatment with mitomycin C (spleen cells) or with an excess dose of ConA (thymocytes) led to sharp reduction in acid DNase activity concomitant with marked drop in thymidine uptake. The results obtained suggest that rise in acid DNase activity takes place during the process of lymphocyte activation by mitogens.

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Classification of cancer chemotherapeutic drugs according to their ability to potentiate contact sensitivity to dinitrofluorobenzene.

The anticancer chemotherapeutic drugs cyclophosphamide (CY), melphalan (L-phenylalanine mustard; L-PAM), 5-fluorouracil (5-FU), methotrexate (MTX), and daunorubicin (DAU) were tested for ability to potentiate contact sensitization (CS) to dinitrofluorobenzene (DNFB) in mice and to inhibit induction of unresponsiveness to such sensitization by preceding exposure to dinitrobenzenesulfonate (DNBS). Administration of CY and L-PAM but not of 5-FU, MTX, and DAU, after DNBS treatment (and before DNFB sensitization) reduced the degree of unresponsiveness effected by DNBS. It is suggested that the test system of CS might be utilized for screening the ability of cancer chemotherapeutic agents to act as nonspecific immuno-modulators.

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Effectiveness of low-dose melphalan treatment against a nonimmunogenic primary induced mouse plasmacytoma.

The fourth i.p. passage of the plasmacytoma "PR" induced by repeated i.p. injections was used for testing chemotherapy with melphalan. The development of "PR" ascitic tumours was slower and the survival time of inoculated mice was longer than that of MOPC-315 inoculated mice. Moreover, the myeloma protein secreted by the "PR" tumour cells, differed from MOPC-315 secreted myeloma protein in its electrophoretic mobility (fast gamma-2) and its characteristics as IgG immunoglobulin. Chemotherapy by a single injection of melphalan 7.5 mg/kg was effective in preventing the development of both MOPC-315 ascitic tumours and "PR" ascitic tumours. Mice cured from MOPC-315 tumours, however, developed antitumour response as shown by resistance to challenge with a high tumourigenic dose and by development of cytotoxic response in vitro against MOPC-315 tumour cells by spleen cells taken from the cured mice. On the other hand, mice cured from "PR" tumour by melphalan were highly susceptible to challenge and their spleen cells were not able to develop a cytotoxic response in vitro against target "PR" tumour cells.

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Inhibition of specific binding of DNP (dinitrophenyl) determinant to lymphoid-cell receptors by related and unrelated compounds : quantitative studies in vitro.

The effect of related and unrelated compounds on the specific binding of dinitrophenyl-coupled bacteriophage (DNP-T4) to lymphoid cell receptors has been examined and compared with the effect on the neutralization of DNP-T4 by anti-DNP serum. Spleen cells and sera from Balb/c mice immunized with DNP-bovine serum albumin were used. The binding of DNP-T4 to the cells was inhibited by DNP-eAcp, di-DNP-Lys, DNP-Tyr, DNP-p(Ornith) and DNP-BSA (among the DNP-derivatives tested), TNP-BSA, ARS-p(Tyr) and TGA. In addition with the above named DNP and TNP compounds, the DNP-T4neutralization by antiserum was also prevented by DNP-derivatives with either L-cysteic acid, alanine, glutamine or poly-L-glutamic acid, while ARS-p(Tyr) and TGA were not effective. Plain carriers (BSA, HSA, poly-ornithine, polylysine and polyglutaminc acid) and cell-mitogens (ConA, LPS and PPD) had no significant inhibitory effect. The results obtained indicate the occurrence of differences between cell-bound receptors and circulating antibodies in what concerning their specific reaction with the dinitrophenyl determinant.

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Activation in vitro of peritoneal macrophages by a nocardia fraction.

The Nocardia fraction NLD-RB1040 (Nocardia Lysozyme Digest) induced cytostatic activity in vitro against the YAC-1 tumor-cell line, in resident murine peritoneal macrophages isolated from BALB/c mice. The induction of antitumor activity by the Nocardia fraction was not correlated with induced changes in production of TNF alpha, PGE2 or nitrite by human peritoneal macrophages collected from renal patients on Continuous Ambulatory Peritoneal Dialysis (CAPD), or changes in production of TNF a by murine macrophages.

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Induction of macrophage antitumor activity by a mycobacterial fraction. In vivo and in vitro studies.

A Methanol Extraction Residue (MER) of BCG tubercle bacillus induced cytostatic activity in vitro against the murine tumor-cell lines YAC-1 and MOPC-315 in resident murine peritoneal macrophages isolated from BALB/c mice. The induction of antitumor activity was not associated with increase in release of TNF-alpha. Macrophages from mice hyperimmunized with MER (MER 3x) or from mice injected once with MER in aqueous suspension released more PGE2 following stimulation in vitro with LPS. Macrophages cultured with either MER or MER+LPS prolonged the survival time of mice bearing palpable RPC5 plasmacytoma s.c. tumors.

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Asialo-positive cells are overexpressed whereas IL-2 induced LAK activity is impaired in mice hyperimmunized with an immunomodulating mycobacterial fraction.

Previously reported studies revealed that extensive immunization with the Methanol Extraction Residue (MER) of BCG tubercle bacillus in Incomplete Freund's Adjuvant (IFA) induced marked suppression of T and B cell functions and that immunosuppression was correlated with marked decrease in splenic T-cell population and marked increase in the splenic macrophage population. The purpose of the present work was to determine if extensive immunization with MER in IFA also induced changes in splenic asialo antigen positive (NK) population and in the potential of induction of splenic LAK activity in vitro by recombinant IL-2. By comparison with other test groups, namely mice injected with IFA only, injected once with MER in aqueous suspension and normal, untreated mice, hyperimmunization with MER resulted in marked increase in expression of asialo positive (NK) splenic cells whereas induction of splenic LAK activity by IL-2 was markedly depressed. Splenic macrophages originated from MER hyperimmunized mice had no effect on induction of LAK activity by IL-2 in a normal splenic population.

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Release of immunosuppressive factor(s) by MOPC-315 murine plasmacytoma cells: a possible mechanism of defence.

Supernatants were collected from suspensions of MOPC-315 tumor cells harvested from ascitic tumors and kept for 24 hours in culture medium and from cultures of an MOPC-315 tumor-cell kept for a long period of time in vitro. The MOPC-315 supernatants were tested for immunosuppression of mitogenic stimulation of BALB/c spleen cells by ConA or LPS, of allogeneic response of effector BALB/c spleen cells against target C57BL spleen cells, of generation of antibody response against SRBC and of induction of LAK activity. The immunosuppression was marked in all the test systems, was not related to secretion of either C-type particles or of anti-TNP antibodies and was also induced by MOPC-315 tumor cells kept in serum-free medium. It is suggested that release of immunosuppressive factor(s) by MOPC-315 tumor cells might play a role in the mechanism(s) of defence of the tumor against the host.

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Secretion of suppressor factors by EBV infected B cell lines.

The infection of human peripheral blood B cells with Epstein-Barr Virus (EBV), induced the production of suppressor factor(s) which were released into the supernatant of the B-cell cultures. The induction of suppressive activity was independent of T-cell presence. The suppression was exhibited both against T-cell activity (MLR and mitogenic stimulation) as well as against B-cell mitogenic stimulation of human or murine B lymphocytes. The suppressive factor(s) was of a low molecular weight (equal or less than 5,000), resistant to trypsin and heating at 80 degrees C and its activity was partially inhibited by neuraminidase treatment. These findings indicate that the suppressive factor(s) is not correlated to immunoglobulin production, is not apparently of a protein nature, and might be of ganglioside or siaylated glycoprotein structure. Our present findings suggest that, in addition to T cells, B cells might also play an immunoregulatory role in the expression of immune response potential.

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Cancer immunotherapy: hopes and pitfalls: a review.

Cancer immunotherapy (IT) started approximately 100 years ago with attempts to use a prepared immune serum against osteosarcoma. Since then, IT was attempted by use of various immunopotentiating agents like whole bacterial cells, bacterial cell fractions, cytokines and thymic humoral factors. The therapeutic efficiency of IT alone was limited and erratic. Accordingly, combined IT with other procedures were used. This included use of "immunomodulating" anticancer drugs as cyclophosphamide (CY) and melphalan (L-PAM) and use of IT in combination with tumor-reducing procedures like surgery, radiation and chemotherapy. The use of immunomodulating drugs was based on findings showing that CY and L-PAM enhance the ability of the immune system to react against tumor cells, in addition to their antitumor activity. Combined treatments were employed with the aim to reduce tumor-burden and as such, render IT more effective. Other therapeutic procedures consisted on use of specific antitumor antibodies as a vehicle for carrying radioactive lethal amounts to tumor cells, use of macrophages activated against tumor cells, use of prostaglandin antagonists and use of specific antitumor vaccines. The general conclusion is that while IT might have some beneficial therapeutic effect especially in conjunction with other procedures, it might be not sufficient to insure cure but it might increase the survival time and improve the quality of life of cancer patients.

Antineoplastic Combined Chemotherapy Protocols↗