Patients with fibrosing alveolitis have active inflammation within their lung interstitium. Previous studies have focused on the humoral (immune complex) driven processes. In this study increased pulmonary gamma interferon production has been evaluated. Bronchoalveolar lavage cells were obtained from 40 patients with fibrosing alveolitis, 22 with cryptogenic fibrosing alveolitis, and 18 with connective tissue disease associated (CTD) fibrosing alveolitis. Increased gamma interferon production was seen in 12 (30%) patients and was similar in the two study groups. Up to 512 units/10(6) cells were released over 24 hours, showing that the amounts of gamma interferon released could be as large as those seen in other pulmonary diseases associated with active cellular immune processes, such as sarcoidosis. Spontaneous gamma interferon production was related to increased serum concentrations of IgG and IgM but not to serum IgA, antinuclear antibody, or rheumatoid factor titres. There was no relation between gamma interferon production and pulmonary uptake of gallium-67 citrate. The ratio of helper-inducer (Leu-3) to suppressor-cytotoxic (Leu-2) cells in bronchoalveolar lavage fluid was similar in the two study groups and was similar in patients whose cells produced gamma interferon and those whose cells did not. These data suggest that gamma interferon is released in the lungs of a proportion of individuals with cryptogenic fibrosing alveolitis and CTD-fibrosing alveolitis, suggesting a role for this cytokine in mediating these diseases.
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