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 (51)Cr 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 [(3)H]
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.