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Published on: October 2, 2015
The characterization of peritoneal and pleural exudate cells from malignant effusions
1Second Department of Surgery, Yamaguchi University School of Medicine, Japan.
Insights
Immune cells in cancer effusions show reduced cytotoxic and NK cell activity, with increased suppressor T-cells. Local interleukin-2 administration can induce lymphokine-activated killer (LAK) cells, suggesting a dual approach for effective immunotherapy.
Area of Science:
- Immunology
- Oncology
- Cell Biology
Background:
- Patients with advanced cancer often exhibit altered immune cell function.
- Malignant effusions can harbor immune cells with distinct characteristics compared to peripheral blood.
Purpose of the Study:
- To compare the immune function of cells from malignant effusions with peripheral blood cells.
- To investigate lymphocyte subsets, natural killer (NK) cell activity, and anti-Daudi and lymphokine-activated killer (LAK) cell activity.
Main Methods:
- Analysis of lymphocyte subsets (CD4+, CD8+CD11+, CD8+CD11-) in peripheral blood mononuclear cells (PBMC) and effusion cells (PEC).
- Measurement of NK cell activity and anti-Daudi activity in PBMC and PEC.
- Induction of LAK cells by culturing with interleukin-2 (IL-2).
Main Results:
- Higher percentage of CD4+ cells in PEC compared to PBMC.
- Increased suppressor T-cells (CD8+CD11+) in PEC and PBMC of patients; cytotoxic T-cells (CD8+CD11-) were similar.
- Lower NK activity in PEC than PBMC; anti-Daudi activity was markedly low in PEC.
- High LAK cell activity was inducible from PEC with IL-2.
Conclusions:
- Immune cells in malignant effusions may have depressed function due to low cytotoxic T-cells, low NK activity, and increased suppressor T-cells.
- Local IL-2 administration can induce LAK cells in malignant effusions.
- Effective immunotherapy for malignant effusions requires augmenting effector cells and inhibiting suppressor cells.
Abstract:
The immune function of peripheral blood cells and cells from the pleural and abdominal effusions of patients with advanced cancer was compared to that of peripheral blood cells from controls. The parameters examined included lymphocyte subsets, natural killer (NK) cell activity, and anti-Daudi and lymphokine-activated killer (LAK) cell activity. The percentage of CD4+ pleural and peritoneal exudate cells (PEC) was significantly higher than the percentage of peripheral blood mononuclear cells (PBMC) in the patients. The percentage of CD8+CD11+ PEC and PBMC, being the suppressor T-cells, of the patients was increased compared with controls, while the percentage of CD8+CD11- PEC, being the cytotoxic T-cells, was identical to the PBMC of both patients and controls. The NK activity of PEC was significantly lower than that of PBMC in both patients and controls, and there was no correlation between the NK activity of PBMC and PEC. Although the anti-Daudi activity of PEC was markedly low, LAK cells with high activity could be induced by culture with interleukin-2 for 4 days. These results suggest that the immune function of cells in malignant effusions may be depressed due to a low population of cytotoxic T cells, low NK activity and increased suppressor T cells, while the local administration of interleukin-2 may induce LAK cells. Therefore, effective local immunotherapy for malignant effusions should not only augment effector cells, but also inhibit suppressor cells.
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