Mechanisms of macrophage activation by corynebacterium parvum. II. In vivo experiments.
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Biomedical subjects
Publications and source records attributed to R Bomford.
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The relative efficiency of active nonspecific or specific immunotherapy of developing methylcholanthrene induced fibrosarcomata with C. parvum was compared. For nonspecific immunotherapy, mice were challenged with tumour cells s.c. or i.v., and 2 days later injected i.v. with dilutions of C. parvum. The only significant effect was a retardation of s.c. tumour growth by the highest concentration of C. parvum (350 mug). However, active specific immunotherapy, using mixtures of C. parvum and irradiated or living tumour cells in the footpads, suppressed tumour growth when given at 2 or 6, but not 10, days after tumour challenge. Successful therapy required: sufficient tumour cells (greater than or equal to 5 X 10(4)); an optimal dose of C. parvum (5-120 mug, increasing with the number of tumour cells); an intact T cell system; the same tumour cells for challenge and treatment. The specificity was confirmed in a protection system in which treatment was given 7 days before tumour challenge. No protective immunity could be achieved with mixtures of C. parvum and foetal cells. Thus in this system C. parvum potentiates protective immunity only to the tumour unique TSTA.
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After i.v. injection of glucans (yeast cell walls, lentinan and pseudonigeran) into CBA mice, the peritoneal macrophages became cytostatic to R1 leukemia cells in vitro, and the mice showed resistance to lung nodule formation by i.v. injected T3 fibrosarcoma cells. The glucans were less active than C. parvum. None of the glucans reproducibly acted as an adjuvant when mixed with irradiated tumour cells; nor did they inhibit the growth of a subcutaneous tumour when injected i.v. or directly into the tumour.