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Cross-reacting antigens in chemically induced sarcomas are fetal determinants
Abstract:
Serologic cross-reactivity has been demonstrated among three MCA-induced sarcomas in C57BL/6N female mice (MCA-2, MCA-3, and MCA-12) with a microcytotoxicity assay. Serum from mice bearing MCA-3 tumor was cytotoxic to both MCA-2 and MCA-3 tumor cells at a titer of 1:8. Sequential absorptions of this serum with syngeneic embryo cells completely eliminate cytotoxicity against MCA-2 cells without affecting the cytotoxic titer against MCA-3 cells. Serum hyperimmune to the MCA-3 tumor reacted with MCA-3, MCA-2, and MCA-12 tumors. Absorption of this serum with embryo cells eliminated cytotoxicity against MCA-2 and MCA-12 cells, but was incapable of lowering the titer against MCA-3 cells below 1:40. Similarly, serum hyperimmune to MCA-2 tumor was lytic to MCA-2, MCA-3, and MCA-12 before absorption, but was lytic only to MCA-2 cells after absorption with sygeneic embryo cells. Thus, the in vitro cross-reactivity between MCA-induced sarcomas is due to a common fetal antigen(s), which is distinct from the individual tumor-specific antigens of each tumor. Since these tumors do not exhibit cross-reactivity in in vivo challenge experiments, it appears that this fetal antigen is not responsible for in vivo immune protection.
Insights
Serologic cross-reactivity in methylcholanthrene-induced sarcomas suggests a common fetal antigen. This shared antigen, detected in vitro, does not confer in vivo immune protection against these tumors.
Area of Science:
- Immunology
- Oncology
- Cancer Research
Background:
- Methylcholanthrene (MCA)-induced sarcomas in C57BL/6N mice exhibit complex antigenic profiles.
- Understanding cross-reactivity among tumors is crucial for developing effective cancer immunotherapies.
Purpose of the Study:
- To investigate the serologic cross-reactivity among three MCA-induced sarcomas (MCA-2, MCA-3, MCA-12).
- To identify the nature of antigens responsible for observed in vitro cross-reactivity.
- To determine if these antigens play a role in in vivo immune responses.
Main Methods:
- Microcytotoxicity assays were performed using sera from tumor-bearing mice.
- Sequential absorption experiments with syngeneic embryo cells were conducted to differentiate antigens.
- In vitro cytotoxicity was assessed against tumor cells before and after absorption.
Main Results:
- Serum from MCA-3 tumor-bearing mice showed cytotoxicity against MCA-2 and MCA-3 cells.
- Absorption with embryo cells removed cytotoxicity against MCA-2 but not MCA-3 cells, indicating distinct antigens.
- Similar results were observed with serum hyperimmune to MCA-2, suggesting a common fetal antigen responsible for in vitro cross-reactivity.
Conclusions:
- In vitro cross-reactivity between MCA-induced sarcomas is mediated by a common fetal antigen(s).
- This common antigen is distinct from individual tumor-specific antigens.
- The identified fetal antigen does not appear to be responsible for in vivo immune protection, as evidenced by a lack of cross-reactivity in challenge experiments.