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Variant mouse lymphoma cells with modified response to interferon demonstrate enhanced immunogenicity
1Department of Cell and Animal Biology, Hebrew University of Jersualem, Israel.
Cancer Immunology, Immunotherapy : CII
|July 1, 1997
Summary
Interferon (IFN) treatment enhances the immunogenicity of non-tumorigenic lymphoma cells by affecting endogenous mouse mammary tumor virus (MMTV) structures. This novel xenogenization method shows promise for improving cancer immunotherapy against various tumors.
Area of Science:
- Immunology
- Virology
- Oncology
Background:
- Developed an experimental model for xenogenization of malignant lymphoma using S49 mouse lymphoma cells.
- Selected non-tumorigenic adherent variants (T-25-Adh) from tumorigenic suspension cells (T-25).
- T-25-Adh cells demonstrated protective immunity against T-25 cells in syngeneic mice.
Purpose of the Study:
- Investigate the effects of interferon (IFN) on endogenous mouse mammary tumor virus (MMTV) structures.
- Determine the impact of IFN on the immunogenicity of T-25-Adh cells.
- Explore IFN as a novel method for lymphoma cell xenogenization.
Main Methods:
- Utilized mouse alpha and beta interferons to treat T-25 and T-25-Adh cells.
- Selected high-responder and low-responder variants based on IFN effects.
- Performed immunoelectron microscopy to analyze MMTV-related antigen interactions.
Main Results:
- IFN affected intracellular MMTV precursor morphogenesis in T-25-Adh cells, but not T-25 cells.
- High-responder variants showed significantly greater protection against T-25 cells.
- Antisera from mice immunized with T-25-Adh cells specifically interacted with cell-surface MMTV budding particles.
Conclusions:
- IFN treatment represents a novel approach for xenogenizing lymphoma cells.
- MMTV-related antigens are crucial for the host immune response to T-25-Adh cells.
- This IFN-mediated xenogenization strategy may be applicable to a broad range of tumors due to endogenous retroviral presence.