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  • 1
    ISSN: 1437-160X
    Keywords: Chondrocyte ; Immune complex ; Cartilage ; Degradation ; Complement ; Cytotoxicity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cartilage from patients with rheumatoid arthritis and from animals with antigen-induced arthritis is frequently contaminated with complement-containing immune complexes. A possible role for complement activation in cartilage degradation was modeled in vitro by exposing cultured bovine chondrocytes to homologous serum, and determining cytotoxicity by monitoring the release of intracellular 51Cr. Complement activation was found to be cytotoxic, having maximal effect at 20–30% serum by 18 h. Serum toxicity was ablated by heat (50°C, 20 min) or methylamine treatment but not by EGTA, suggesting that in these experiments activation occurred by the alternate route. The implications of the results are discussed in relation to ultrastructural evidence for the involvement of complement in the pathogenesis of cartilage degradation in inflammatory arthritis.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Rheumatology international 8 (1988), S. 47-53 
    ISSN: 1437-160X
    Keywords: Rabbit ; Tenosynovitis ; Antigen ; Tendon ; Rheumatoid arthritis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rabbits were first immunized and later challenged with the same antigen (bovine serum albumin, or ferritin) by injection into the tibialis anterior tendon. Inflammatory changes of the tenosynovium and epitenon included infiltration by neutrophils (early) and mononuclear cells (later) over a 6-week course of tenosynovitis. A pattern of antigen entrapment in the tendon together with immunoglobulin was shown by use of radiolabelled antigen and immunochemical staining. Half-life of antigen in the tissues averaged 5 days over the 6-week period. Changes in the epitenon included cellular necrosis, appearance of phagocytic cells, and disruption of the collagen matrix. Tissues of control animals (challenged without prior immunization) showed minimal changes and significantly less retention of antigen (P〉0.005). The model is relevant to the mechanism of tendon damage associated with antigen-driven chronic inflammation, as may be the case in rheumatoid arthritis.
    Type of Medium: Electronic Resource
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