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Research Article Free access | 10.1172/JCI107215

Immunopathologic Studies in Relapsing Polychondritis

Jerome H. Herman and Marie V. Dennis

Division of Immunology, Department of Internal Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio 45229

Find articles by Herman, J. in: PubMed | Google Scholar

Division of Immunology, Department of Internal Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio 45229

Find articles by Dennis, M. in: PubMed | Google Scholar

Published March 1, 1973 - More info

Published in Volume 52, Issue 3 on March 1, 1973
J Clin Invest. 1973;52(3):549–558. https://doi.org/10.1172/JCI107215.
© 1973 The American Society for Clinical Investigation
Published March 1, 1973 - Version history
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Abstract

Serial studies have been performed on three patients with relapsing polychondritis in an attempt to define a potential immunopathologic role for degradation constituents of cartilage in the causation and/or perpetuation of the inflammation observed. Crude proteoglycan preparations derived by disruptive and differential centrifugation techniques from human costal cartilage, intact chondrocytes grown as monolayers, their homogenates and products of synthesis provided antigenic material for investigation. Circulating antibody to such antigens could not be detected by immunodiffusion, hemagglutination, immunofluorescence or complement mediated chondrocyte cytotoxicity as assessed by 51Cr release. Similarly, radiolabeled incorporation studies attempting to detect de novo synthesis of such antibody by circulating peripheral blood lymphocytes as assessed by radioimmunodiffusion, immune absorption to neuraminidase treated and untreated chondrocytes and immune coprecipitation were negative.

Delayed hypersensitivity to cartilage constituents was studied by peripheral lymphocyte transformation employing [3H]thymidine incorporation and the release of macrophage aggregation factor. Positive results were obtained which correlated with periods of overt disease activity. Similar results were observed in patients with classical rheumatoid arthritis manifesting destructive articular changes. This study suggests that cartilage antigenic components may facilitate perpetuation of cartilage inflammation by cellular immune mechanisms.

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