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Immunopathologic studies in relapsing polychondritis.

J H Herman, M V Dennis

    The Journal of Clinical Investigation
    |March 1, 1973
    PubMed
    Summary
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    Cellular immunity may drive relapsing polychondritis inflammation. This study found delayed hypersensitivity to cartilage components in patients, suggesting a role for cellular immune mechanisms in cartilage inflammation.

    Area of Science:

    • Immunology
    • Rheumatology
    • Cellular Biology

    Background:

    • Relapsing polychondritis (RP) is an autoimmune disease characterized by episodic inflammation of cartilaginous tissues.
    • The precise immunopathogenesis of RP remains incompletely understood, particularly the role of cartilage-specific antigens.

    Purpose of the Study:

    • To investigate the potential immunopathologic role of cartilage degradation products in the causation and perpetuation of inflammation in relapsing polychondritis.
    • To assess both humoral and cellular immune responses to cartilage constituents in patients with RP.

    Main Methods:

    • Serial studies were performed on three RP patients.
    • Antigenic material was derived from human costal cartilage, including proteoglycans, intact chondrocytes, and their synthetic products.

    Related Experiment Videos

  • Humoral immunity was assessed using immunodiffusion, hemagglutination, immunofluorescence, and complement-mediated cytotoxicity assays.
  • Cellular immunity was evaluated through peripheral lymphocyte transformation assays (using [3H]thymidine incorporation) and assessment of macrophage aggregation factor release.
  • Similar assessments were conducted in patients with rheumatoid arthritis (RA) exhibiting destructive articular changes.

    • Main Results:

    • No circulating antibodies to cartilage antigens were detected in RP patients.
    • No de novo synthesis of antibodies by peripheral blood lymphocytes was observed.
    • Positive delayed hypersensitivity responses to cartilage constituents were found in RP patients, correlating with disease activity.
    • Similar positive cellular immune responses were observed in RA patients with destructive arthritis.

    Conclusions:

    • This study suggests that cellular immune mechanisms, specifically delayed hypersensitivity to cartilage antigenic components, may play a significant role in the perpetuation of cartilage inflammation in relapsing polychondritis.
    • Cartilage-specific antigens may act as triggers or perpetuators of inflammation through T-cell mediated immune responses.