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Dissociation between tumour resistance and delayed-type hypersensitivity to tumour-associated antigens in the mouse
Abstract:
A comparison was made in mice between resistance to growth of a syngeneic methylcholanthrene-induced fibrosarcoma (Meth A) and specific delayed-type hypersensitivity to this tumour. Resistance could be induced in 90% of mice following a single injection of 10(4) Meth A cells. This resistance could be transferred by spleen cells but not serum. Delayed skin reactivity to ultrasonicated Meth A cells was found in both tumour-resistant and tumour-bearing mice and could be passively transferred by spleen cells and serum. These findings suggest a dissociation between tumour resistance and specific delayed-type hypersensitivity. It would appear that, in this system, delayed skin reactivity to Meth A tumour cells is mediated by humoral antibody despite a mononuclear cell infiltrate at 24 and 48 h and that this could be the reason for its lack of correlation with host resistance to tumour growth which is cell-mediated and not transferable by serum.
Insights
Tumor resistance in mice was transferable via spleen cells, not serum. Delayed hypersensitivity, transferable by both cells and serum, showed no correlation with tumor resistance.
Area of Science:
- Immunology
- Oncology
- Tumor immunology
Background:
- Investigating the relationship between host immune responses and tumor growth is crucial for developing effective cancer therapies.
- Methylcholanthrene-induced fibrosarcoma (Meth A) in mice provides a model to study tumor-specific immunity.
Purpose of the Study:
- To compare tumor resistance with delayed-type hypersensitivity in a syngeneic mouse model.
- To elucidate the mechanisms underlying tumor resistance and delayed-type hypersensitivity.
Main Methods:
- Induction of tumor resistance in mice using Meth A fibrosarcoma cells.
- Transfer experiments using spleen cells and serum to assess immune mediators.
- Assessment of delayed-type hypersensitivity via skin reactivity tests.
Main Results:
- A single injection of Meth A cells induced resistance to tumor growth in 90% of mice.
- Tumor resistance was transferable by spleen cells but not by serum.
- Delayed skin reactivity was observed in both tumor-resistant and tumor-bearing mice and was transferable by spleen cells and serum.
Conclusions:
- A dissociation exists between tumor resistance and specific delayed-type hypersensitivity.
- Delayed skin reactivity in this model appears to be mediated by humoral antibodies, not cell-mediated immunity.
- Host resistance to tumor growth is cell-mediated and not transferable by serum, explaining the lack of correlation with delayed hypersensitivity.