Abstract
Pulmonary berylliosis, a chronic allergic pneumosclerosis resulting from inhalation of beryllium compounds, may occur in two clinical forms: interstitial, which is mild, slowly progressive, and presents moderate skin reactions of delayed-type hypersensitivity to haptens; and granulomatous, which is rapidly progressive after a short latent period and presents systemic lesions and significant allergic skin reactions. The investigation of experimental berylliosis in rats has revealed some factors that could lead to the abolition of natural tolerance. Six new beryllium-containing autoantigens, two of which accumulated in different tissues, were identified in the lung nucleoproteins accompanying a partial loss of normal tissue and serum antigens. Antibodies to the new antigens and to normal lung tissue (in smaller amounts) were found in the sera of rats with experimental berylliosis, as well as in patients. The patients with granulomatous berylliosis also had antibodies to DNA, RNA, and extracts of normal homologous heart, spleen, liver, and thyroid in quantities that correlated with the clinical picture and with the effectiveness of glucocorticoid therapy. The fact that natural tolerance mechanisms were interrupted in all cases and autoimmune granulomatous berylliosis developed only in some patients led to the assumption that the mechanism was effective under the influence of additional endogenous factors; diseases producing an accumulation of autoantibodies could provide the stimulus for the appearance of these factors.
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