Related Experiment Videos
Decrease of transplantability by the immunopotentiators, OK-432 and interleukin-2: experiments on a human hepatoma
H Saito1, T Morizane, Y Inagaki
1Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
European Journal of Cancer & Clinical Oncology
|January 1, 1989
Summary
Immunopotentiators like OK-432 and human interleukin-2 enhance spleen cell cytotoxic activity, inhibiting hepatoma tumor growth in mice. This resistance is mediated by natural killer cells and other non-specific cytotoxic cells.
Area of Science:
- Immunology
- Oncology
- Cancer Research
Background:
- Nonspecific cytotoxic activity of spleen cells is crucial for tumor resistance.
- Understanding the role of these cells in hepatoma graft challenges is important.
Purpose of the Study:
- To investigate the relationship between spleen cell cytotoxicity and resistance to human hepatoma cell line (HCC-M) grafts in nude mice.
- To determine the role of natural killer cells and other cytotoxic cells in this process.
Main Methods:
- Administration of immunopotentiators (OK-432 or human interleukin-2) prior to HCC-M cell inoculation.
- Assessment of tumor development (tumor take rate and size).
- Evaluation of spleen cell cytotoxicity against YAC-1 or HCC-M targets.
- Inhibition studies using anti-asialo GM1 (ASGM1) antiserum and in vitro treatment.
Main Results:
- Immunopotentiators significantly inhibited tumor development.
- The inhibitory effect was abrogated by anti-ASGM1 antiserum, indicating the involvement of ASGM1+ cells.
- A significant inverse correlation was observed between tumor volume and spleen cell cytotoxicity.
- Enhanced cytotoxicity involved heterogeneous cells, including ASGM1+ natural killer cells and other non-specific cytotoxic cells.
Conclusions:
- Nonspecific cytotoxic cells play a critical role in resistance against tumor cell challenge.
- The level of cytotoxic activity at the time of tumor cell challenge is a key determinant of tumor development.
- Immunopotentiators can enhance this resistance through modulation of non-specific cytotoxic cells.