Phenotypes and lymphokine-activated killer activity of pleural cavity lymphocytes of lung cancer patients without malignant effusion.
We examined the phenotypes of lymphocytes in the pleural cavity of 23 lung cancer patients without malignant effusion. The ability of those lymphocytes to develop lymphokine-activated killer (LAK) activity and the regulation of LAK by pleural cavity macrophages were also compared with their counterparts in the peripheral blood. Mononuclear cells (MNC) were obtained simultaneously from the blood and by lavage of the pleural cavity of patients with lung cancer. The proportion of the T-cell subset of HLA-DR+ cells was significantly higher in the pleural cavity than in the peripheral blood, but the proportions of CD3+ and CD8+ cells in the pleural cavity were similar to the corresponding proportions in the blood. The proportions of CD4+ and CD16+ cells were lower in the pleural cavity than in the blood. The LAK activity could be developed by MNC from the pleural cavity following incubation with interleukin 2 (IL-2), but the LAK activity of pleural cavity MNC was significantly less than that of peripheral MNC. Pleural cavity lymphocytes alone also developed LAK activity following incubation with IL-2. Pleural macrophages from the patients were regulated to augment in vitro induction of LAK activity by IL-2 from autologous blood lymphocytes and pleural cavity lymphocytes. Lymphocytes in the pleural cavity without malignant pleural effusion could be developed by LAK activity and this activity was augmented by pleural cavity macrophages. The LAK activity developed by pleural cavity lymphocytes was significantly lower than that developed by peripheral blood lymphocytes. However, they can change their population to include cells with higher activities on exposure to IL-2 against the invasion of lung cancer cells into the pleural cavity. Thus, the population of lymphocytes in the pleural cavity of patients with lung cancer without malignant pleural effusion was different from that in malignant pleural effusion.
Takahashi
K
K
Second Department of Surgery, School of Medicine, University of Tokushima, Japan.
Sone
S
S
Kimura
S
S
Ogura
T
T
Monden
Y
Y
D000368:Aged; D003602:Cytotoxicity, Immunologic; D005260:Female; D005434:Flow Cytometry; D006684:HLA-DR Antigens / Q000032:analysis; D006801:Humans; D016130:Immunophenotyping; D015979:Killer Cells, Lymphokine-Activated / Q000276:immunology*; D008175:Lung Neoplasms / Q000276:immunology*; D016131:Lymphocyte Subsets; D008264:Macrophages / Q000502:physiology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000502:physiology; D010994:Pleura / Q000276:immunology*; D016066:Pleural Effusion, Malignant / Q000276:immunology*; D015854:Up-Regulation
D006684:HLA-DR Antigens