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R Austgulen

Publications and source records attributed to R Austgulen.

63 records · Page 4Linked to original sources

Monocyte-mediated drug-dependent cellular cytotoxicity: effects on different WEHI 164 target cell lines.

The contribution of monocyte cytotoxic protein factor (CF) to monocyte-mediated drug-dependent cellular cytotoxicity (DDCC) has been investigated. Cell lines which have been derived from murine WEHI 164 cells (termed WEHI 164 parental) by selecting for high (WEHI 164 clone 3) and low (R-WEHI 164) sensitivity to CF-mediated cytotoxicity were used as target cells in DDCC. By comparing the CF doses which produced 50% dead cells (LD 50) we found that WEHI 164 clone 3 was approximately 30 times more sensitive than WEHI 164 parental which in turn was 70 times more sensitive than R-WEHI 164. Actinomycin D (Act D) treatment of WEHI 164 parental and R-WEHI 164 greatly increase susceptibility to CF-mediated cytotoxicity. The susceptibility of WEHI 164 clone 3 was apparently somewhat increased at low dilutions of CF, whereas no significant increase was observed at high dilutions. The susceptibility to DDCC of the three target cell lines (WEHI 164 parental, WEHI 164 clone 3, and R-WEHI 164) correlated with the sensitivity pattern obtained in CF-mediated cytotoxicity of Act D-treated target cells. Monocyte- and CF-mediated cytotoxicity against Act D-treated WEHI 164 clone 3 and R-WEHI 164 was inhibited by neutralizing CF antiserum. These data indicate that CF is an effector molecule in monocyte-mediated DDCC.

Animals↗

Human monocyte cytotoxic factor mediates cytolysis of WEHI 164 cells.

Human monocytes can be activated to release a 40,000-Da cytostatic protein factor (CF). In this report we have investigated the cytolytic activity of CF on WEHI 164 cells which are sensitive to monocyte-mediated cytolysis. Monocyte supernatants containing CF induced cytolysis of murine WEHI 164 sarcoma cells, as determined in a 51Cr-release assay. Preincubation of WEHI 164 cells with actinomycin D enhanced cytolysis induced by supernatants containing CF, suggesting that CF may be involved in drug-dependent cellular cytotoxicity. The cytolytic activity was profoundly inhibited by a rabbit antiserum raised against purified CF, indicating that the cytolytic activity in the supernatants was in fact mediated by CF. These results indicate that CF may be an important effector molecule in monocyte-mediated cytostatic and cytolytic reactions.

Adjuvants, Immunologic↗

Role of monocyte cytotoxic factor in cytolysis of actinomycin D-treated WEHI 164 cells mediated by freshly isolated human adherent mononuclear blood cells.

The role of the monocyte cytotoxic factor (CF) in cytolysis of untreated and actinomycin D (Act D)-treated WEHI 164 cells by freshly isolated human adherent mononuclear cells has been investigated in this study. Murine WEHI 164 cells were used as target cells because of their sensitivity to lysis mediated by monocytes and their resistance to natural killer cells. Monocytes as well as monocyte supernatants mediated cytolysis of WEHI 164 cells. Cytolysis was enhanced by Act D treatment of target cells. The addition of lipopolysaccharide to monocytes accelerated the progression of cytolysis of Act D-treated WEHI 164 cells mediated by monocytes. A polyclonal rabbit antiserum against CF inhibited the cytolytic activity of monocytes and monocyte supernatants against untreated as well as Act D-treated WEHI 164 cells. At low effector:target ratios, the cytolysis was totally abrogated by CF antiserum. Depletion of natural killer cells from adherent cells by the monoclonal antibody Leu 11b and rabbit complement did not reduce cytolysis of Act D-treated WEHI 164 cells. Immunofluorescence microscopy revealed that CF antiserum stained the plasma membrane of freshly isolated monocytes, suggesting that CF is a membrane-associated molecule. Our data indicate that CF is an important effector molecule in cytolysis mediated by freshly isolated monocytes against untreated and Act D-treated WEHI 164 cells.

Animals↗

Immunization of children with malignant diseases with the Oka-strain varicella vaccine.

Twenty children with different malignancies were vaccinated using an Oka-strain varicella vaccine (Varilrix) obtained from Smith Kline-RIT. Until now, no serious side effects to the vaccine have been observed and none of the vaccinees have had a varicella infection during this period. Nine children have been tested for cell-mediated immune responses against varicella antigen. Antibodies against varicella have been measured using an enzyme-linked immunosorbent assay technique. Tests were performed 4 weeks, 6 and 12 months after vaccination; at 4 weeks, 85% of the children had seroconverted, but by 12 months, those patients who were negative before vaccination had no detectable antibodies. While the blastogenic lymphocyte response to varicella antigen gradually increased during the first year after vaccination, it was much lower than after natural infection. The results indicate the need for revaccination, probably within 6 months after the first vaccination.

Antibodies, Viral↗