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Biomedical subjects

A Santoni

Publications and source records attributed to A Santoni.

At least 181 records · Page 10Linked to original sources
PubMed1980

Cytotoxic effector cells with the characteristics of natural killer cells in the lungs of mice.

Cells with in vitro cytotoxicity against tumor targets in a short-term 51Cr release assay have been recovered from the lungs of mice that were either untreated or injected with biological or synthetic agents 1--3 days earlier. The cytotoxic effector cells were non-adherent, non-phagocytgic and shared many characteristics with splenic natural killer (NK) cells. This finding is discussed with particular regard to our previous observations on the rapid in vivo elimination from the lungs of intravenously injected, radiolabelled tumor cells.

Adjuvants, Immunologic↗
PubMed1980

Effects of adriamycin on the activity of mouse natural killer cells.

Adriamycin, a widely employed anti-neoplastic agent, was found to have either inhibitory or stimulatory effects on NK activity, depending on the site examined. A single i.p. administration of ADM resulted in a rapid increase of cytolytic activity by PEC of various mouse strains. The effector cells appeared to be NK cells, being nonadherent and nonphagocytic; they expressed low amounts of Thy 1.2 antigen and had the same pattern of specificity as splenic NK cells. In contrast to the stimulatory effects of NK activity of PEC, ADM caused a transient dose-dependent depression of NK activity in the spleen, with a peak reduction at day 3 and recovery within a few days thereafter. The depressed NK activity could be reversed by removal of adherent cells by passage through a nylon column. Moreover, ADM induced cytostatic activity against tumor cells by macrophages, suggesting that activated macrophages may be responsible for suppression of splenic NK activity. The possible modulation of the levels of NK activity by ADM-induced macrophages was supported by mixture experiments, in which plastic adherent spleen cells from ADM-treated mice, but not from normal mice, inhibited the NK activity of normal spleen cells.

Animals↗
PubMed1979

Activation of mouse macrophages by pyran copolymer and role in augmentation of natural killer activity.

Inoculation of mice with pyran copolymer resulted in activation of natural killer (NK) cells as well as macrophages. Conditions optimal for the boosting of NK activity seemed to differ from those optimal for macrophage activation as assessed by cytostasis of tumor target cells. Peak levels of macrophage cytostatic reactivity were found at about 7 days after drug injection and were only achieved by the highest doses of pyran tested. Macrophage activation was consistently higher in the peritoneal cavity than in the spleen, regardless of route of administration, in contrast to the failure of i.v. pyran to induce high NK reactivity in peritoneal exudate cells. At 2-3 days after pyran treatment of older mice, NK augmentation reached peak levels, but only minimal macrophage activation was found. Despite these differences, macrophages played a role in regulating NK activity in pyran-treated mice. Functional macrophages appeared to be required for augmentation of NK activity by pyran, since boosting was impaired by prior in vivo inoculation of silica. Macrophages also appeared able to inhibit NK activity. In younger mice that exhibited high spontaneous levels of NK activity, pyran treatment produced a substantial reduction in NK activity to levels below those of untreated mice. This depression coincided with the time of peak levels of macrophage cytostasis. Furthermore, removal of adherent cells from the spleen cells of these pyran-treated mice resulted in levels of NK activity almost as high as those of untreated mice. The possibility that the depression of NK activity in young mice by pyran copolymer is due to suppressor cells is discussed.

Animals↗
PubMed1979

Augmentation of natural killer activity by pyran copolymer in mice.

Treatment of older mice with pyran copolymer, a known interferon-inducer, was found to result in a rapid boosting of cell-mediated cytolytic activity against YAC-1 tumor target cells. The effector cells were characterized as being non-adherent and were presumed to be natural killer (NK) cells. Augmentation occurred in various lymphoid organs and was detectable 2-3 days after drug treatment. Differences in the levels of boosted activity among the lymphoid organs resulted when the route of administration was varied. The degree of augmentation was largely independent of the dose of pyran, but did vary among different strains of mice. Augmentation, moreover, was followed by a rapid decline by 5-7 days.

Adjuvants, Immunologic↗
PubMed1979

Adriamycin-induced antitumor response in lethally irradiated mice.

Lethally irradiated mice pretreated with a wide range of Adriamycin (ADM) doses were tested for their in vivo antitumor response against transplanted lymphoma cells. Tumor growth, as assessed by 125IUdR uptake, was markedly impaired by treatment with ADM by a variety of different administration schedules. This ADM-induced antitumor response was largely dose-dependent, occurred regardless of route of administration, and was detectable as late as 15-30 days following drug treatment. No genetic restriction could be found to regulate the development of this response, since tumor growth inhibition occurred in syngeneic as well as allogeneic tumor-host combinations. ADM-induced antitumor response did not appear to be due to direct antitumor action by the drug, but rather to some interaction with host immune mechanisms. Antimacrophage agents, such as silica or carrageenan, abrogated the response. The possible implication of different cells as effectors of this response is discussed.

Animals↗
PubMed1979

Correlation between natural and antibody-dependent cell-mediated cytotoxicity against tumor targets in the mouse. II. Characterization of the effector cells.

Direct comparison of the effector cells mediating natural killer (NK) activity against mouse tumor cells and antibody-dependent cell-mediated cytotoxicity (ADCC) against mouse tumor target cells coated with alloantisera indicated that NK cells and K-cells (effector cells mediating ADCC) may belong to the same subpopulation of lymphocytes, but they have a different mechanism of killing. Effector cells mediating NK activity and ADCC were nonadherent, nonphagocytic Fc receptor-bearing cells that sediment at 3.5-4.5 mm/hour. Treatment with anti-Thy 1.2 serum in the absence of complement resulted in an increase of NK activity, whereas this treatment caused a substantial loss in ADCC. Both NK activity and ADCC were equally sensitive to the in vivo or in vitro effects of X-irridiation. In vivo inoculations of high doses of hydrocortisone resulted in a reduction of NK activity, but ADCC was not affected. NK cells were trypsin-sensitive, with a profound decrease in the cytolytic activity being observed in a 4-hour 51Cr release assay. The activity, however, could be recovered after overnight incubation at 37 degrees C. Trypsin treatment did not inhibit ADCC as measured by the 18-hour assay.

Animals↗
PubMed1979

Rapid in vivo assay of mouse natural killer cell activity.

A rapid elimination of tumor cells from some organs was detected in mice following iv injection of tumor cells labeld in vitro with [125I]5-iodo-2'-deoxyuridine. Recovery of radioactivity in different organs (spleen, liver, and lungs) was reduced in mice with high natural killer (NK) cell reactivity in their spleens, as measured in vitro by concomitant short-term 51Cr release assay. Considerable parallelism between in vitro and in vivo reactivities against two mouse lymphomas and a human myeloid cell line was found in mice of different strains and ages. Similarly, various immunophamacologic treatments had comparable effects on in vitro and in vivo reactivities. These findings are consistent with the hypothesis that rapid cytolysis of tumor cells occurred in vivo and that NK cells played a major role in their elimination.

Age Factors↗
PubMed1978

Secondary cytotoxic response in vitro against Moloney lymphoma cells antigenically altered by drug treatment in vivo.

Cell-mediated cytotoxic response in vitro to a Moloney strain of murine leukemia virus-induced tumor (LSTRA) altered by 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide (DTIC) was investigated with the use of mixed-leukocyte tumor cell cultures (MLTC). As assessed by means of a short-term 51Cr-release assay, minimal or no cytolytic activity was generated in primary MLTC. In contrast, high specific cytotoxic response against the altered tumor was obtained in secondary MLTC. Partial cross reactivity was found between the LSTRA and LSTRA/DTIC tumor lines.

Animals↗