Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1973 Mar;52(3):549-58.
doi: 10.1172/JCI107215.

Immunopathologic studies in relapsing polychondritis

Immunopathologic studies in relapsing polychondritis

J H Herman et al. J Clin Invest. 1973 Mar.

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 (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.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Br J Exp Pathol. 1967 Feb;48(1):66-80 - PubMed
    1. Int Arch Allergy Appl Immunol. 1966;30(1):58-66 - PubMed
    1. J Clin Invest. 1971 Feb;50(2):266-73 - PubMed
    1. Trans Assoc Am Physicians. 1968;81:249-57 - PubMed
    1. Lancet. 1969 Aug 2;2(7614):246-7 - PubMed