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For comparison, 18 control subjects and 7 patients with active pulmonary sarcoidosis were also studied. Recovered BAL cells were cultured for 24 h (5 \u00d7 106\/ml), and the supernatant was assayed for interferon by determining inhibition of cytopathic effect on encephalomyocarditis virus-induced lysis of WISH cells and characterized by monoclonal anti-IFN\u03b3 antibody inhibition. Nine (35%) patients with asbestosis released increased amounts of IFN\u03b3, up to 320 units\/ml, the levels seen in the sarcoidosis patients. All control subjects released \u2a7d10 units\/ml. All interferon released was IFN\u03b3. In asbestosis patients, IFN\u03b3 production was not related to a history of cigarette smoking, there was no significant difference in the ratio of helper\/inducer (Leu-3) to suppressor\/cytotoxic (Leu-2) cells in IFN\u03b3 producers compared to non-IFN\u03b3 producers (p &amp;gt; 0.05), and IFN\u03b3 production correlated significantly with serum IgG levels (p &amp;lt; 0.001) but not with the levels of IgM, IgA, antinuclear factor, or rheumatoid factor. These data suggest that active cellular immune processes are present in the lungs of a proportion of patients with asbestosis.<\/jats:p>","DOI":"10.1164\/ajrccm\/138.2.278","type":"journal-article","created":{"date-parts":[[2013,4,4]],"date-time":"2013-04-04T16:58:21Z","timestamp":1365094701000},"page":"278-283","source":"Crossref","is-referenced-by-count":17,"title":["Increased Pulmonary Gamma Interferon Production in Asbestosis"],"prefix":"10.1093","volume":"138","author":[{"given":"Bruce W. 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