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T Boon

Publications and source records attributed to T Boon.

At least 199 records · Page 11Linked to original sources
PubMed1982

Protection against a nonimmunogenic mouse leukemia by an immunogenic variant obtained by mutagenesis.

The nonimmunogenic thymic leukemia TH, obtained in mouse strain CBA/Ht, was adapted to culture. By in vitro treatment of a clonal TH cell line with the mutagen N-methyl-N'-nitro-N-nitrosoguanidine, stable variant cell clones (tum-) were obtained that elicited a rejection response in syngeneic mice. Mice that had rejected a tum- variant were partially protected against a challenge with the original tumor. When spleen cells of these animals were restimulated in vitro, cytolytic T cells were obtained that were directed against an antigen present on the original tumor. The existence of these cytolytic effectors was confirmed by clonal analysis of the cytolytic response. No immune protection against TH was observed in mice that had been immunized with irradiated cells of the original TH tumor. These results confirm that tum- variants can elicit a syngeneic rejection response against tumors that are apparently devoid of transplantation immunogenicity. The experimental conditions and the results make it likely but not certain that the tumor-associated antigen detected on leukemia TH was present on the primary tumor.

Animals↗
PubMed1981

Stimulation of cytolytic T lymphocytes by azaguanine-resistant mouse tumor cells in selective HAT medium.

Primed syngeneic or unprimed allogeneic mouse spleen cells were stimulated with azaguanine-resistant P815 tumor cells that were killed by the addition of aminopterin to the stimulation medium. The recovery of lymphocytes and their cytolytic activity and specificity were similar to those obtained after stimulation with irradiated cells. This method conveniently replaces the inactivation of stimulatory cells by irradiation or mitomycin treatment. Moreover, it has the advantage of inactivating not only the stimulatory cells but also the tumor cells that often contaminate the spleens of tumor-bearing animals, provided these animals have been inoculated with azaguanine-resistant tumor cell mutants.

Aminopterin↗
PubMed1980

Immunogenic variants obtained by mutagenesis of mouse mastocytoma P815. I. Rejection by syngeneic mice.

We have reported that it is possible to obtain variants that are incapable of forming progressive tumour in syngeneic mice (tum-) by mutagenesis and cloning of a teratocarcinoma and a Lewis lung carcinoma cell line. These observations were extended to the ascitic P815 mastocytoma of mouse strain DB/2. After a treatment with the mutagen N-methyl-N"-nitro-N-nitrosoguanidine, we obtained a high frequency (14%) of tum- clones. A colony assay indicated that after a period of rapid multiplication extending to approximately 10 d after injection, the P815 tum- cells were rejected by a process that was usually completed by day 15. No rejection was observed in sublethally irradiated animals. The immunological nature of the rejection of the P815 variants was further inferred because, upon rejection, the mice acquired a radioresistant specific protection that could be transferred adoptively with spleen cells. Cross-immunization patterns demonstrated the presence of singular antigenic specificities on three of the five variants that were examined. In addition, a common antigen was found on all the tum- variants and the original cells that were capable of forming progressive tumors in syngeneic mice (tum+). Mice injected with tum- cells were significantly protected against a tum+ challenge, even though no significant protection was generated by irradiated tum+ cells. A study of the T lymphocyte-mediated cytolysis against the P815 variants described here is presented in the accompanying report (9).

Animals↗
PubMed1980

Immunogenic variants obtained by mutagenesis of mouse mastocytoma P815. II. T lymphocyte-mediated cytolysis.

Tumor cell variants that were rejected by syngeneic mice (tum-) were obtained from mastocytoma P815 by mutagenesis (as described in the accompanying report (13). A considerable T lymphocyte-mediated lysis was observed upon incubation of these tum- variants with peritoneal exudate cells collected a few days after an intraperitoneal challenge of immune animals. Spleen cells from these animals were cytolytic after stimulation in vitro with the immunizing variant. New antigens, absent from the original P815 tum+ cells, were detected on 15 of the 21 tum- variants that were tested. All these antigens appeared to be different. No new antigen was detected on any of 10 mutagenized P815 clones that had retained their ability to form tumors. We compared the evidence obtained in vivo and in vitro for the presence of specific antigens on five tum- variants. Three variants were shown both in vivo and in vitro to carry an individual antigen. One showed no specificity either in vivo or in vitro. However, for one variant, no specificity was observed in vivo, although cytolysis tests demonstrated the existence of a singular antigenic specificity.

Animals↗
PubMed1979

Tumor cell variants obtained by mutagenesis of a Lewis lung carcinoma cell line: immune rejection by syngeneic mice.

It has been reported that, by mutagenesis of a malignant mouse teratocarcinoma cell line, it is possible to obtain cell variants that are incapable of forming progressive tumors in syngeneic mice. These variants, which were called "tum-," are eliminated from the host by an immune rejection process. We report here that similar variant cell clones can be obtained at high frequency from a Lewis lung carcinoma cell line treated with the mutagen N-methyl-N'-nitro-N-nitrosoguanidine. Syngeneic C57BL/6 mice reject these tum- clones and acquire a strong radioresistant immune protection against the immunizing clone. When the challenging tum- clone differs from the immunizing clone, a weaker radioresistant immune protection can be demonstrated with some, but not all, combinations. All the tum- clones induce a significant protection against the original Lewis lung malignant cells. These results imply that each Lewis lung tum- variant carries on its surface a singular antigen in addition to one or more weak antigens already present on the original tumor cell line. This antigenic pattern is similar to that found on teratocarcinoma tum- variants. Our results suggest that the procedure of using a mutagen in order to generate tum- variants carrying new transplantation antigens may be generally applicable to cancer cells.

Animals↗
PubMed1978

Teratocarcinoma cell variants rejected by syngeneic mice: protection of mice immunized with these variants against other variants and against the original malignant cell line.

We reported previously that, by mutagenesis of a malignant teratocarcinoma cell line, it is possible to obtain a number of variant clones that are incapable of forming progressive tumors. Each of these "tum-" variants is rejected in syngeneic mice and stimulates the production of immune memory cells (self-protection). We show here that four different tum- clones confer an immune protection against each other although this cross-protection is invariably weaker than the self-protection. Moreover, mice immunized with living tum- cells are partially protected against the original malignant teratocarcinoma cells, even though the latter cells are incapable of conferring any immune protection when injected after being killed by irradiation. These results indicate that each tum- variant carries at least one specific transplantation antigen that is absent from the original tumor cell line and from most other tum- variants. Other tumor-specific transplantation antigens are probably present on all the tum- variants and also on the malignant teratocarcinoma cell line.

Animals↗
PubMed1977

Rejection by syngeneic mice of cell variants obtained by mutagenesis of a malignant teratocarcinoma cell line.

Cells from the malignant teratocarcinoma line PCC4.azal were treated with the mutagen N-methyl-N'-nitro-N-nitrosoguanidine. Fifty-five clones were isolated from the surviving cells. Twelve clones are unable to form tumors in the syngeneic 129/Sv mice. However, these "tum-" clones form tumors as readily as the original cells when they are injected into irradiated mice. Moreover, they stimulate the production of immune memory cells, which protect the injected animals and confer resistance by adoptive transfer. The tum- clones are therefore unable to generate tumors in syngeneic mice because they elicit an immune rejection response.

Animals↗
PubMed1972

Inactivation of ribosomes in vitro by colicin E 3 and its mechanism of action.

The incubation of purified ribosomes with colicin E(3) results in the cleavage of a terminal fragment from the 16S ribosomal RNA. The cleavage reaction requires three components: colicin E(3), the 30S ribosomal subunit, and the 50S ribosomal subunit. An immunity factor found in extracts derived from colicinogenic cells prevents the in vitro inactivation of ribosomes by colicin E(3). Evidence is presented suggesting that it does so by binding to the colicin molecule. The mode of action of colicin E(3)in vivo can be explained by the assumption that a small fraction of the adsorbed colicin penetrates into the cell and catalytically inactivates the ribosomes.

Antigen-Antibody Reactions↗
PubMed1971

Inactivation of ribosomes in vitro by colicin E 3 .

Cell-free protein synthesizing extracts incubated with purified preparations of colicin E(3) showed a marked decrease of their protein synthesizing activity. Incubation of ribosomes prepared from S-30 extracts with E(3) resulted in their inactivation. Their 16S RNA was found to lose a terminal fragment, similar in size to the fragment released upon in vivo treatment with E(3). Extracts derived from colicinogenic strains are resistant to the action of E(3)in vitro.

Autoradiography↗