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Immunomodulation in an apparently non-immunogenic murine tumor
I Bursuker1, B A Petty, K M Neddermann
1Bristol-Myers Squibb Pharmaceutical Research Institute, Bristol-Myers Squibb Company, Wallingford, CT 06492.
International Journal of Cancer
|September 30, 1991
Summary
This study demonstrates that the Madison lung carcinoma (M109) tumor, initially appearing non-immunogenic, can elicit anti-tumor immunity. Immunopotentiation reveals a T-cell-dependent response, suggesting tumor-induced immunosuppression rather than absent antigens.
Area of Science:
- Immunology
- Oncology
- Tumor Biology
Background:
- The Madison lung carcinoma (M109) is a murine tumor model that appears non-immunogenic using standard assays.
- Tumor-induced immunosuppression can mask the presence of tumor-associated antigens and hinder effective anti-tumor immunity.
Purpose of the Study:
- To investigate the immunogenicity of the M109 tumor model.
- To explore the role of immunopotentiation in overcoming apparent non-immunogenicity.
- To determine if tumor-associated antigens are present despite initial non-immunogenicity.
Main Methods:
- Utilized C.parvum to induce immunopotentiation in M109 tumor-bearing mice.
- Assessed post-excision anti-tumor immunity through tumor implant challenges.
- Employed adoptive immunotherapy and passive T-cell transfer experiments.
Main Results:
- C.parvum-induced immunopotentiation led to measurable post-excision anti-tumor immunity against M109.
- The observed immunity was tumor-specific and T-cell-dependent.
- T cells from excised tumor-bearing mice could inhibit immunotherapy in recipients, suggesting the presence of tumor antigens.
Conclusions:
- The apparent non-immunogenicity of M109 is likely due to tumor-induced immunosuppression, not a lack of antigens.
- Shifting the immune balance towards effector mechanisms via immunopotentiation can reveal anti-tumor responses.
- This model highlights the importance of considering immune balance in cancer immunology research.