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Characterization of T lymphocytes mediating in vivo protection against RSV-induced murine sarcomas
Abstract:
Tumors induced by Rous sarcoma virus (RSV) in different mouse strains share a common tumor-associated transplantation antigen, whose expression is controlled both by the viral transforming src gene and by cellular gene(s) (Prat et al., 1981). The mechanism(s) responsible for the in vivo protective immune response against two RSV-induced sarcomas has now been investigated. In the "Winn assay" the growth of both tumors was specifically prevented or significantly reduced by the simultaneous administration of lymphocytes isolated from immunized donors. The effector cells were radiosensitive (2,500 rad), Lyt-1+, Lyt-2,3+ Thy.1+ cells. Better protection was afforded by transfer of immune spleen cells from mice pretreated with cyclophosphamide, which is known to abrogate T-cell suppressor activity. In a 5-day mixed lymphocyte/tumor cell culture specific anti-RSV-induced sarcoma cytotoxic activity was barely detected, while a good production of interferon-gamma (IFN-y) was observed. The cells involved showed the same functional and surface phenotype as displayed by the effectors of the "Winn" assay. It is concluded that in the immune rejection of RSV-induced sarcomas, Lyt-1+, Lyt-2,3+ T cells, rather than cytotoxic T lymphocytes, and lymphokines such as IFN-gamma are involved.
Insights
Immune rejection of Rous sarcoma virus (RSV)-induced tumors involves Lyt-1+, Lyt-2,3+ T cells and interferon-gamma (IFN-γ). These cells, rather than cytotoxic T lymphocytes, mediate protection against RSV sarcomas.
Area of Science:
- Immunology
- Virology
- Oncology
Background:
- Rous sarcoma virus (RSV)-induced tumors express a common tumor-associated transplantation antigen.
- This antigen's expression is regulated by the viral src gene and cellular genes.
- The in vivo immune mechanisms against RSV-induced sarcomas require further investigation.
Purpose of the Study:
- To investigate the cellular mechanisms underlying the protective immune response against RSV-induced sarcomas in vivo.
- To identify the specific immune cell populations and mediators involved in tumor rejection.
Main Methods:
- Utilized the Winn assay to assess the anti-tumor activity of lymphocytes from immunized donors.
- Characterized effector cells by their radiosensitivity and surface markers (Lyt-1+, Lyt-2,3+, Thy.1+).
- Evaluated cytotoxic activity and interferon-gamma (IFN-γ) production in mixed lymphocyte/tumor cell cultures.
Main Results:
- Lymphocytes from immunized donors specifically prevented or reduced tumor growth in the Winn assay.
- Effector cells were identified as radiosensitive Lyt-1+, Lyt-2,3+, Thy.1+ T cells.
- Significant IFN-γ production was observed, with minimal cytotoxic T lymphocyte activity detected.
Conclusions:
- The immune rejection of RSV-induced sarcomas is primarily mediated by Lyt-1+, Lyt-2,3+ T cells, not cytotoxic T lymphocytes.
- Lymphokines, particularly IFN-γ, play a crucial role in this anti-tumor immune response.
- Cyclophosphamide pretreatment enhanced protective immunity, suggesting the involvement of suppressor T cells.