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M R Price

Publications and source records attributed to M R Price.

At least 163 records · Page 9Linked to original sources
PubMed1978

Circulating immune complexes in rats bearing chemically induced tumours. II. Characterization of sera from different stages of tumour growth.

Sera from rats bearing intraperitoneal implants of an aminoazo dye-induced hepatoma were fractionated by Sephadex G200 and DEAE-cellulose ion exchange column chromatography. Isolated fractions were examined for their capacity to bind [125I]C1q as a measure of immune complex levels, and for their ability to bind soluble tumour-specific antigen as well as to react with antigens expressed at the surface of viable hepatoma cells. Elevated levels of circulating immune complexes in unfractionated serum were directly detectable during early tumour development although, following serum fractionation, immune complexes were identified at both early and late stages of tumour growth. The present findings suggest that the detection of immune complexes in unfractionated samples of late tumour-bearer serum using a C1q-binding assay is masked by the increasing production of tumour-specific antibodies and by a shift from complement fixing to non-complement-fixing tumour-specific antibodies.

Animals↗
PubMed1978

Circulating immune complexes in rats bearing chemically induced tumors. I. Sequential determination during the growth of tumours at various body sites.

Circulating immune complexes were measured in sequential monitoring studies in rats bearing chemically induced tumours at different body sites. The assay employed were based upon radioimmunoprecipitation of serum factors with 125I-C1q or with an indirect test whereby the inhibition of binding of 125I-C1q to IgG aggregates by tumour-bearer sera was measured. 125I-C1q-binding immune complexes were detected at the initial phase of tumour growth and the level of this activity returned to the normal range after tumour excision. With tumour growing at subcutaneous sites or in th peritoneal cavity, serum-borne C1q-binding material, after reaching a maximum level, decreased despite tumour progression and eventually fell into sub-normal ranges at terminal stages of growth. In contrast, following intravenous tumour cell injection, immune-complex levels increased until terminal stages of disease. The present findings indicate that the measurement of C1q-binding serum factors represents a useful method for monitoring the growth and burden of experimental animal tumours.

Animals↗
PubMed1977

Tumour-specific complement-dependent serum cytotoxicity against a chemically induced rat hepatoma.

A short-term 51Cr release test was used for the detection of complement-dependent cytolytic activity of syngeneic serum for transplanted aminoazo dye-induced rat hepatoma cells in suspension. Serum samples from rats bearing intraperitoneal implants of one hepatoma (hepatoma D23) were specifically cytotoxic for hepatoma D23 target cells, although this activity was not detected in sera from donors bearing subcutaneous tumour grafts. Other sera containing demonstrable IgG antibodies reactive in membrane immunofluorescence tests with individually distinct tumour-specific antigens or tumour-associated embryonic antigens were not cytotoxic for hepatoma D23 cells; and even though serum from donors carrying intraperitoneal tumour grafts contained tumour-specific IgG antibody, the complement-dependent reactivity was confined to the 19s region of fractionated tumour-bearer serum. These findings are discussed in relation to the development of humoral responses in the tumour-bearing host and with regard to the significance of the availability of an objective and reproducible assay for measuring humoral responses directed against the tumour-specific antigens associated with chemically induced rat tumours.

Animals↗
PubMed1977

Evaluation of 51Cr release for detecting cell-mediated cytotoxic responses to solid chemically induced rat tumours.

A 51Cr-release test was developed for the detection of cell-mediated cytotoxicity against transplanted solid chemically induced rat tumours, and the findings were compared with those obtained in parallel tests using a microcytotoxicity assay. It was necessary to incorporate several modifications of the original Brunner assay (Brunner et al., 1968) in order to increase the sensitivity of the test as applied to long-term tumour lines maintained as glass-adherent cultures. These included: 1. preincubation of labelled tumour cells at 37 degrees C for 3-4 h before addition of effector cells; 2. preincubation of effector cells at 37 degrees C for 12 h before addition to target cells; 3. upon admixture of target and effector cells, intimate cell contact was established by gentle centrifugation; 4. after incubation of target and effector cells at 37 degrees C, a further incubation for 1 h at 45 degrees C was included to complete the release of 51Cr from non-viable cells. Maximal cytotoxicity of tumour-bearer effector cells was detected after 12 h incubation of lymphoid and target cells at a ratio of 200:1. Spleen cells from tumour-bearing rats during the first 2 weeks of tumour growth exhibited the same pattern of reactivity in the 51Cr-release test and the microcytotoxicity assay, although significant reduction in target-cell numbers was more frequently recorded using the microcytotoxicity assay. Tumour-bearer spleen cells showed reactivity against the homologous tumour as well as against unrelated tumours. Using either assay, pre-exposure of effector cells to 3M KC1 extracts of tumour was found to inhibit their effect on tumour cells most frequently in tests in which the effector-cell donor, soluble extract and target cell were of the same tumour line.

Animals↗
PubMed1976

Inhibition of cell-mediated cytotoxicity to chemically induced rat tumours by soluble tumour and embryo cell extracts.

When lymph-node and spleen cells from rats bearing or immunized against aminoazo dye-induced rat hepatomas or 3-methylcholanthrene-induced rat sarcomas were pretreated with 3 M KCl extracts of these tumors, their cytotoxicity for cultured cells from the corresponding tumour was specificially inhibited. In cross-test combinations of target tumour and tumour-bearer effector-cell donor, tumour extracts only inhibited cytotoxic responses when they were derived from the tumour homologous to the target-cell and not when the extract was from the tumour borne by the effector-cell donor. One component of the tumour-bearer cytotoxic response was shown to be directed against tumour-associated embryonic antigens since soluble extracts of embryos or tumour extracts containing embryonic antigens inhibited tumour-bearer cell-mediated cytotoxicity in both specific and cross-test combinations of target tumour and effector cells. These findings are discussed in relation to tumour antigen expression and the immune responses that these tumour-associated antigens may evoke in tumour-bearing rats.

Animals↗
PubMed1975

Cell-mediated cytotoxicity to chemically-induced rat tumours.

Cell-mediated immune reactions against carcinogen-induced rat tumours were demonstrated by the in vitro microcytotoxicity test. Lymph-node cells from syngeneic rats immunized against individual aminoazo-dye-induced hepatomas or 3-methylcholanthrene-induced sarcomas were cytotoxic for cells of the immunizing tumour compared with the effects of normal lymph-node cells. Only a low level of cross-reactivity was detectable against target cells derived from otherr tumours. Conversely, lymph-node cells from tumour -bearing rats were cross-reactive against a range of tumour cells, suggesting that the tumour-bearer was sensitized against a common antigen(s) as well as the individually specific antigen associated with these tumours. Lymph-node cells were reactive at an early time (from day 2) after tumour implantation and their cytotoxic potential persisted until terminal stages of tumour growth. Spleen cells from tumour-bearer and tumour-immune donors also exhibited comparable cytotoxic reactivities of the same specificity as that shown by lymph-node cell preparations. These findings are discussed in relation to the development of cell-mediated immune responses in the tumour-bearing rat and in immunized rats which are capable of rejecting transplanted tumour cells.

Animals↗