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Biomedical subjects

R C Burton

Publications and source records attributed to R C Burton.

At least 109 records · Page 6Linked to original sources
PubMed1978

Natural cytotoxicity of haemopoietic cell populations against murine lymphoid tumours.

Homozygous nude and normal mice of 3 strains, BALB/c, CBA and C57BL, were used as sources of nucleated haemopoietic "natural killer" (NK) cells. These killer cells could lyse a wide range of syngeneic and allogeneic lymphoid tumour cell lines in vitro, and it was found that cell suspensions from nude mice were always significantly more active than those from normal mice, and that the most active effector population was a polymorph-enriched peritoneal-exudate cell suspension. Eosinophils did not appear to be involved in the phenomenon, and mononuclear peritoneal-exudate cell suspensions were actually highly inhibitory. Three non-lymphoid tumours, a carcinoma, a fibrosarcoma and a mastocytoma, were totally resistant to in vitro lysis. Although all susceptible tumour cell lines were C-type virus-associated, not all of these tumours were killed by all strain sources of spleen cells, indicating a specificity of killing.

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PubMed1978

In vitro induction of tumour-specific immunity V. Detection of common antigenic determinatnts of murine fibrosarcomas.

Two 3-methylcholanthrene and a spontaneous BALB/c fibrosarcoma were examined for tumour-associated antigens (TAA) by in vivo and in vitro induction of tumour-immune responses. When BALB/c mice were immunized to these fibrosarcomas by surgical tumour removal, cross-reacting tumour-associated transplantation antigens (TATA) were detected on all 3 tumours. Cytotoxic effector cells (CL) were then induced in vitro by co-culture of BALB/c spleen cells with the spontaneous, or one of the carcinogen-induced fibrosarcomas. These CL were shown to be cytotoxic T cells (Tc) and to be directed against cross-reacting TAA on all 3 tumours, by two in vitro 51Cr-release assay systems, direct 51Cr-release cytotoxicity and cellular competitive inhibition of 51Cr release. Further studies demonstrated that the fibrosarcoma TAA involved in in vitro induction of Tc were not present on normal adult or foetal tissues. A secondary cytotoxic response was also detected in vitro when spleen cells from mice immunized to a carcinogen-induced fibrosarcoma were tested. The patterns of cross-reactivity detected by the in vivo and primary in vitro tumour-immune responses suggested that the TAA detected in vivo (TATA) were not identical to the TAA detected in vitro.

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PubMed1978

Maternal alloimmunisation in pregnancy. In vitro studies of T cell-dependent immunity to paternal alloantigens.

A secondary in vitro allograft reaction was used to demonstrate that spleen cells derived from allogeneically mated inbred mice were immunised against paternal alloantigens. In addition to the heightened alloantigen-specific in vitro response of these spleen cells, it was also found that spleen cells froma a wide variety of syngeneically and allogeneically mated mice were nonspecifically more reactive in the in vitro allograft reaction than spleen cells from virgin mice. However, when spleen cells freshly harvested from allogeneically mated mice were tested in a direct 51Cr release assay, lysis of target cells bearing the paternal alloantigens was demonstrable in only one-third of the experiments. It is proposed that T cell immunisation to paternal alloantigens occurs in pregnancy, but that cell-mediated cytotoxicity is inhibited.

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PubMed1978

Tumor immunity to murine plasma cell tumours. Influence of responder genotype on the specificity of the immune response to plasmacytomas and T lymphomas.

A tumour-associated antigen has been identified which is expressed on both BALB/c plasmacytomas and T lymphomas, but which does not induce a detectable cell-mediated immune response in the strain of origin of the tumours. The (BALB/c x C57BL) F1 hybrid, however, makes a readily detectable response both in vivo and in vitro in vitro experiments with various BALB/c H-2 F1 cogenic mice indicated that the genetic control of the response was not H-2 linked, and was associated with other C57BL genes.

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PubMed1977

Inhibition of the growth of lymphoid tumours in syngeneic athymic (nude) mice.

A comparison of the growth of a number of BALB/c tumours in BALB/c, BALB/c.nu/ + (heterozygous nude) and BALB/c.nu (homozygous) nude mice has shown that a majority of BALB/c lymphoid tumours grow at a significantly reduced rate in BALB/c.nu mice. The three non-lymphoid BALB/c tumours (carcinomas and sarcomas) tested and a minority of lymphoid tumours, however, grew as well, or better, in the BALB/c.nu mice. Furthermore a correlation, without exception to date, has emerged from a comparison between the susceptibility of a tumour cell line to in vitro lysis by spleen cells from syngeneic nude mice and its growth in vivo in syngeneic nude mice. Only those lymphoid tumour cell lines lysed in vitro show the reduced growth rate in syngeneic nude as compared to syngeneic normal mice. Tumour cell lines, both lymphoid and non-lymphoid, which are resistant to in vitro lysis do not show the reduced in vivo growth rate in syngeneic nude mice. Both the in vivo and in vitro effect can be partially abolished by irradiating the nude mice prior to use, suggesting that a radiation-sensitive non-T-cell surveillance of lymphoid tumours is operating in nude mice. While the identity of the antigens is still unknown, the specificity of the phenomena suggest that C-type RNA oncogenic viral determined antigens are involved.

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PubMed1977

In vitro induction of tumor-specific immunity. VI: analysis of specificity of immune response by cellular competitive inhibition: limitations and advantages of the technique.

The cellular competitive inhibition 51Cr-release assay makes two distinct contributions to the in vitro study of cell-mediated immunity. It allows target cells which are not amenable to isotopic labelling to be investigated for their antigenic specificity, and it provides a means, complementary to the direct cytotoxicity assay, of estimating qualitative and quantitative differences in antigen expression on intact normal and neoplastic cells. Various parameters of a micro-51Cr-release inhibition assay have been studied, and it was found that the assay conditions markedly influenced both the sensitivity and specificity. It is concluded that optimal assay conditions for specificity include: 1) moderate levels of lysis on the linear part of the CL/T titration curve, 2) avoidance of prolonged assay times, and 3) low ratios of blocker to target cells. When tumor cells with large cell volumes are used as competitive inhibitor (blocker) cells, non-specific blocking will occur; limits have been defined for this particular micro-inhibition assay which, in general, exclude these effects.

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PubMed1977

Tumor immunity to murine plasma cell tumors. III. Detection of common and unique tumor-associated antigens on BALB/c, C3H, and NZB plasmacytomas by in vivo and in vitro induction of tumor-immune responses.

Tumor-associated antigens (TAA) were demonstrated on plasmacytomas derived from BALB/c, NZB, and C3H mouse strains, by in vivo and in vitro techniques. By immunizing the appropriate F1 hybrid mice with these tumors, it was possible to show that all the plasmacytomas expressed cross-reactive tumor-associated transplantation antigens. When cytotoxic lymphocytes (CL) were induced in vitro by the coculturing of syngeneic or F1 hybrid spleen cells with irradiated plasmacytoma cells, "shared" and "unique" plasmacytoma TAA were demonstrable. This was accomplished by inducing CL in vitro against one syngeneic plasmacytoma and assaying for lytic activity on a range of 51Cr-labeled BALB/c, NZB and C3H plasmacytoma cells in vitro. In a second in vitro assay, unlabeled plasmacytoma cells were tested for their ability to inhibit the lysis of a particular 51Cr-labeled plasmacytoma, with the use of CL induced in vitro against it. The possibility that these TAA were "self" antigens was excluded by demonstrating in the inhibition assay that they were not present on T lymphomas and spleen cells of the same strain, and that CL "autosensitized" in vitro could not significantly lyse 51Cr-labeled plasmacytoma cells in vitro. From both in vivo and in vitro studies of immunity to these tumors, it was concluded that any one plasmacytoma line possesses multiple TAA of both shared and unique types.

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PubMed1977

In vitro induction of tumor-specific immunity. III. Lack of requirement for H-2 compatibility in lysis of tumor targets by T cells activated in vitro to oncofetal and plasmacytoma antigens.

Many recent studies have demonstrated that cytotoxic T lymphocytes (CL) activated to various antigens other than those of the H-2 complex, will lyse target cells only when H-2 compatibility exists between the CL and target cell. From these observations, it has been inferred that T lymphocytes might only be capable of responding to H-2 antigen or antigens that become associated with H-2 region gene products. Our results suggest that this is not the case, and that in some situations, cytotoxic T lymphocytes can specifically lyse target cells of different H-2 types. Two in vitro systems are described where primary induction of cytotoxic T lymphocytes to oncofetal and plasmacytoma antigens results in CL capable of lysing suitable targets bearing these antigens, of either syngeneic or allogeneic derivation. Thus it is proposed that although interaction antigens involving H-2 components may preferentially activate T lymphocytes, this does not imply a restriction on the recognition potential of T lymphocytes.

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PubMed1976

In vitro induction of tumor-specific immunity. II. Activation of cytotoxic lymphocytes to murine oncofetal antigens.

The presence of oncofetal antigens (OFA) on a wide variety of murine tumor cells was demonstrated to a totally in vitro system of cellular immunity. Nonimmune spleen lymphocytes were cocultivated with irradiated syngeneic fetal liver cells and, at various times after initiation of culture, were tested for the presence of cytotoxic lymphocytes (CL) by 51Cr-release assay with labeled tumor target cells. Significant cytotoxic activity was regularly detected after such culture, whereas only minor levels appeared in control cultures of spleen lymphocytes with irradiated syngeneic spleen cells. Specificity of the reaction was assessed by inhibition tests in which nonlabeled cells were admixed to the CL and 51Cr-labeled tumor targets. Fetal liver cells gave significant inhibition; however, no inhibition was found with adult spleen cells. Various tumor types gave inhibition, and fibrosarcomas were more effective than plasmacytomas or lymphomas. The results suggested that all tumor types tested possess such OFA, as well as their unique or virus-associated, tumor-associated transplantation antigens, and that the in vitro system permits a more active response to the tumor-associated OFA than that observed in in vivo studies.

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PubMed1976

Analysis of murine oncofetal antigens as tumor-associated transplantation antigens.

In previous studies with in vitro activated cytotoxic T lymphocytes, we have demonstrated the presence of oncofetal antigens (OFA) on a range of murine tumor cells. The present studies with the same tumor lines attempt to determine whether these antigens are also capable of activating lymphocyte responses in vivo. Several experimental designs were followed, each being performed many times (1). Preimmunization of mice with irradiated fetal liver cells and followed by challenge with viable tumor cells did not consistently produce a state of tumor resistance. However, injection of live fetal cells frequently led to enhanced tumor growth (2). The growth of tumors in multiparous mice can be inhibited, in contrast to controls, but this effect was relatively short lived after parturition (3). Preimmunization with fetal cells in vivo did not result in augmented secondary cytotoxic T cell responses in vitro (4). Immunization of mice with irradiated tumor cells frequently led to a state of resistance to the clonal growth of hemopoietic fetal cells, although again the level of resistance was usually relatively weak. From the overall results, we conclude that OFA are relatively poor immunogens on tumor cells or fetal cells in vivo, and in contrast to in vitro responses, do not act as potent tumor transplantation antigens.

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PubMed1975

Prophylactic use of gentamicin in colonic and rectal surgery.

A double-blind trial was performed to test whether a single intramuscular injection of 80 mg of gentamicin would significantly reduce the incidence of septic complications of elective colonic and rectal surgery. The gentamicin was given at the time of anaesthetic premedication, the operations were performed by either of two surgeons, and the patients were followed up by an independent investigator. Eighty patients satisfactorily completed the trial. There was no significant difference in the incidence of postoperative wound infection, intraperitoneal abscess formation and faecal fistula between the 41 patients who received the gentamicin and the 39 who received the placebo. However, the mortality was significantly lower in the gentamicin group, in which there was only one death.

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