UNLABELLED: IFN-gamma a potent antifibrotic activity in interstitial lung diseases (ILD). T cells, both Th1 and Tc1, are considered to be the main local source of IFN-gamma. MATERIAL AND METHODS: BAL fluids of 98 patients with ILD, incl. idiopathic pulmonary fibrosis (IPF/UIP), sarcoidosis, extrinsic allergic alveolitis (EAA), asbestosis and silicosis (n=16, 49, 7, 10, 16 resp.) were tested with ELISA for IFN-gamma levels. Results were compared with BAL cytoimmunology and patients' clinical data. RESULTS: Significantly increased IFN-gamma levels were found in non-treated patients with EAA (7.8 +/- 2.1), IPF (6.1 +/- 1.8), Loefgren's syndrome, LS (11.9 +/- 2.6) and progressive sarcoidosis, PS (6.4 +/- 1.2, p < 0.05 for all), whereas the results in pneumoconioses were comparable to those obtained in controls (2.0 +/- 1.1 pg/ml, median +/- SEM). IFN-gamma results were positively correlated with total number of CD4+ cells (r(s) = +0.38, p < 0.05), CD4+ cells percentage (r(s) = +0.32, p < 0.005) and CD4+/CD8+ ratio (r(s) = +0.38, p = 0.0007), but negatively correlated with CD8+ cell percentage (r(s) = -0.39, p < 0.0005). In IPF patients with CD4/CD8 < or =1 (n=9) IFN-gamma level was lower as compared with the group with CD4/CD8 >1 (n=7), 2.8 +/- 1.3 vs. 7.3 +/- 1.0 pg/ml. In sarcoidosis, IFN-gamma level did not seem to have a prognostic role, since values obtained in PS did not differ remarkably from those in stable sarcoidosis and LS. Moreover, subsequent steroid treatment in 7 patients with progressive sarcoidosis did not change significantly IFN-gamma levels in BAL fluid. CONCLUSIONS: Increased IFN-gamma level was found in non-treated patients with IPF, Loefgren's syndrome and progressive sarcoidosis. CD4+ (Th1), but neither CD8+ (Tc1) nor NK cells seem to be the main local source of IFN-gamma in ILD. Relatively low CD4/CD8 ratio in ILD may indicate the patients with increased risk of lung fibrosis.
UNLABELLED: IFN-gamma a potent antifibrotic activity in interstitial lung diseases (ILD). T cells, both Th1 and Tc1, are considered to be the main local source of IFN-gamma. MATERIAL AND METHODS: BAL fluids of 98 patients with ILD, incl. idiopathic pulmonary fibrosis (IPF/UIP), sarcoidosis, extrinsic allergic alveolitis (EAA), asbestosis and silicosis (n=16, 49, 7, 10, 16 resp.) were tested with ELISA for IFN-gamma levels. Results were compared with BAL cytoimmunology and patients' clinical data. RESULTS: Significantly increased IFN-gamma levels were found in non-treated patients with EAA (7.8 +/- 2.1), IPF (6.1 +/- 1.8), Loefgren's syndrome, LS (11.9 +/- 2.6) and progressive sarcoidosis, PS (6.4 +/- 1.2, p < 0.05 for all), whereas the results in pneumoconioses were comparable to those obtained in controls (2.0 +/- 1.1 pg/ml, median +/- SEM). IFN-gamma results were positively correlated with total number of CD4+ cells (r(s) = +0.38, p < 0.05), CD4+ cells percentage (r(s) = +0.32, p < 0.005) and CD4+/CD8+ ratio (r(s) = +0.38, p = 0.0007), but negatively correlated with CD8+ cell percentage (r(s) = -0.39, p < 0.0005). In IPF patients with CD4/CD8 < or =1 (n=9) IFN-gamma level was lower as compared with the group with CD4/CD8 >1 (n=7), 2.8 +/- 1.3 vs. 7.3 +/- 1.0 pg/ml. In sarcoidosis, IFN-gamma level did not seem to have a prognostic role, since values obtained in PS did not differ remarkably from those in stable sarcoidosis and LS. Moreover, subsequent steroid treatment in 7 patients with progressive sarcoidosis did not change significantly IFN-gamma levels in BAL fluid. CONCLUSIONS: Increased IFN-gamma level was found in non-treated patients with IPF, Loefgren's syndrome and progressive sarcoidosis. CD4+ (Th1), but neither CD8+ (Tc1) nor NK cells seem to be the main local source of IFN-gamma in ILD. Relatively low CD4/CD8 ratio in ILD may indicate the patients with increased risk of lung fibrosis.