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Cross Regulation by IL-10 and IL-2/IL-12 of the Helper T Cells and the Cytolytic Activity of Lymphocytes From Malignant Effusions of Lung Cancer Patients

Yuh-Min Chen; Wen-Kuang Yang; Den-Mei Yang; Jacqueline Whang-Peng; Chou-Chik Ting; Wen-Ying Tsai; Reury-Perng Perng
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Affiliations: From the Chest Department, Veterans General Hospital-Taipei; and National Health Research Institute, and School of Medicine, National Yang-Ming University, Taiwan, ROC,  From the Cancer Clinical Research Center; and National Health Research Institute, and School of Medicine, National Yang-Ming University, Taiwan, ROC,  From the Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Md.,  From the Chest Department, Veterans General Hospital-Taipei; National Health Research Institute, and School of Medicine, National Yang-Ming University, Taiwan, ROC

Affiliations: From the Chest Department, Veterans General Hospital-Taipei; and National Health Research Institute, and School of Medicine, National Yang-Ming University, Taiwan, ROC,  From the Cancer Clinical Research Center; and National Health Research Institute, and School of Medicine, National Yang-Ming University, Taiwan, ROC,  From the Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Md.,  From the Chest Department, Veterans General Hospital-Taipei; National Health Research Institute, and School of Medicine, National Yang-Ming University, Taiwan, ROC

Affiliations: From the Chest Department, Veterans General Hospital-Taipei; and National Health Research Institute, and School of Medicine, National Yang-Ming University, Taiwan, ROC,  From the Cancer Clinical Research Center; and National Health Research Institute, and School of Medicine, National Yang-Ming University, Taiwan, ROC,  From the Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Md.,  From the Chest Department, Veterans General Hospital-Taipei; National Health Research Institute, and School of Medicine, National Yang-Ming University, Taiwan, ROC

Affiliations: From the Chest Department, Veterans General Hospital-Taipei; and National Health Research Institute, and School of Medicine, National Yang-Ming University, Taiwan, ROC,  From the Cancer Clinical Research Center; and National Health Research Institute, and School of Medicine, National Yang-Ming University, Taiwan, ROC,  From the Laboratory of Immune Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Md.,  From the Chest Department, Veterans General Hospital-Taipei; National Health Research Institute, and School of Medicine, National Yang-Ming University, Taiwan, ROC


1997 by the American College of Chest Physicians


Chest. 1997;112(4):960-966. doi:10.1378/chest.112.4.960
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Abstract

Study objective: Our previous report demonstrated that there was impairment of local cellular immunity with elevated interleukin-10 (IL-10) and undetectable IL-12 in neoplastic pleural effusion. These findings suggest that the local immune reactions favor the T-helper type 2 (Th2) pathway instead of Th1 pathway. The present study was designed to examine whether local cellular immunity could be manipulated by IL-2 and/or IL-12 treatment, and to determine their effect on the helper T-cell pathways and the cytolytic activity of the effusion-associated lymphocytes (EALs).

Design: Using malignant pleural effusions obtained from four patients suffering from adenocarcinoma of lung, we separated the tumor cells from the EALs with Ficol-Hypaque centrifugation, followed by Percoll density centrifugation. To test whether the cytolytic function of lymphocytes could be enhanced by culturing with IL-2 and/or IL-12, lymphocytes were incubated with recombinant IL-2 with/without IL-12 for 6 days. Following this, the tumoricidal activity was assessed in an overnight 51chromium-release assay. Autologous tumor cells for measuring specific antitumor activity, Daudi cells susceptible to lymphokine-activated killer cells, and NK-susceptible K562 cells were used as target cells.

Measurements and results: After treatment in vitro with IL-2, IL-12, or IL-2 plus IL-12, the Th pathway shifted from Th2 to Th1 type (increased γ-interferon production). To further study the effect of cytokine treatment on the cytolytic activity of EALs, it was found that after 6-day culturing, the EALs failed to kill any of the three tumor targets, whereas the 6-day cultured peripheral blood lymphocytes (PBLs) gave low level of cytotoxicity against all three tumor targets. Stimulation with IL-2 alone partially restored the immunocompetence of EALs to kill the tumor targets. Stimulation with IL-12 alone showed no significant effect on their cytolytic activity. However, IL-12 synergized with IL-2 to increase the cytolytic activity of EALs and PBLs against autologous tumor targets. This synergistic effect was not found for Daudi cells and K562 cells.

Conclusions: These results suggest that EALs activated with IL-12 in the presence of a low concentration of IL-2, which converted the EALs from Th2 pathway to Th1 pathway, could be an alternative source of antitumor effectors for adoptive immunotherapy of cancer.


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