PURPOSE: Multiple immune functions such as activation of T cells and monocytes or cytolysis of tumor cells are mediated via the adhesion receptor/ligand pairs CD2/LFA-3 and LFA-1/ICAM-1. Because soluble forms of LFA-3 (sLFA-3) and ICAM-1 (sICAM-1) can interfere with these functions, we asked whether increased levels of sLFA-3 and/or sICAM-1 can be found in malignant or inflammatory effusions compared with transudates. METHODS: sLFA-3 and sICAM-1 levels were measured by enzyme-linked immunoassays in pleural effusions from 70 patients (6 transudates, 10 inflammatory, 47 malignant, and 7 other effusions). Twenty pleural fluid samples were tested in parallel for the complete sLFA-3 molecule or sLFA-3-domain 1 only. RESULTS: Increased levels of sICAM-1 were found in all types of exudates compared with transudates. Highest levels of sICAM-1 were measured in malignant exudates, particularly in effusions caused by mesotheliomas, non-small lung cancers, and gynecologic malignancies. This was also true for sLFA-3. However, sLFA-3 levels were not increased in inflammatory effusions. sLFA-3 levels correlated significantly with protein, cholesterol, lactate dehydrogenase, and sICAM-1 levels. Comparison of sLFA-3-domain 1 and the complete sLFA-3 molecule revealed identical sLFA-3 levels, suggesting the absence of nonfunctional split products. CONCLUSIONS: Elevated levels of the complete sLFA-3 molecule were found in malignant pleural effusions, while sICAM-1 level was elevated in both inflammatory and malignant effusions. Secretion of sICAM-1 and sLFA-3 by tumor cells might block T-cell-mediated immune functions such as tumor cytotoxicity. Alternatively, secretion of soluble adhesion molecules might reflect the generalized inflammation within the pleural space.
PURPOSE: Multiple immune functions such as activation of T cells and monocytes or cytolysis of tumor cells are mediated via the adhesion receptor/ligand pairs CD2/LFA-3 and LFA-1/ICAM-1. Because soluble forms of LFA-3 (sLFA-3) and ICAM-1 (sICAM-1) can interfere with these functions, we asked whether increased levels of sLFA-3 and/or sICAM-1 can be found in malignant or inflammatory effusions compared with transudates. METHODS: sLFA-3 and sICAM-1 levels were measured by enzyme-linked immunoassays in pleural effusions from 70 patients (6 transudates, 10 inflammatory, 47 malignant, and 7 other effusions). Twenty pleural fluid samples were tested in parallel for the complete sLFA-3 molecule or sLFA-3-domain 1 only. RESULTS: Increased levels of sICAM-1 were found in all types of exudates compared with transudates. Highest levels of sICAM-1 were measured in malignant exudates, particularly in effusions caused by mesotheliomas, non-small lung cancers, and gynecologic malignancies. This was also true for sLFA-3. However, sLFA-3 levels were not increased in inflammatory effusions. sLFA-3 levels correlated significantly with protein, cholesterol, lactate dehydrogenase, and sICAM-1 levels. Comparison of sLFA-3-domain 1 and the complete sLFA-3 molecule revealed identical sLFA-3 levels, suggesting the absence of nonfunctional split products. CONCLUSIONS: Elevated levels of the complete sLFA-3 molecule were found in malignant pleural effusions, while sICAM-1 level was elevated in both inflammatory and malignant effusions. Secretion of sICAM-1 and sLFA-3 by tumor cells might block T-cell-mediated immune functions such as tumorcytotoxicity. Alternatively, secretion of soluble adhesion molecules might reflect the generalized inflammation within the pleural space.