Immunization of laboratory rats with native Type II collagen induces arthritis in approximately 40 percent of the individuals. Histological and radiological analysis have suggested that the lesion bears several similarities to human rheumatoid arthritis. Clinical studies conducted with this model indicate that it is responsive to the treatment with clinically-used NSAID's, steroids and immunosuppressive agents. When rats with collagen arthritis were treated with DMARD's, only those treated with D-penicillamine showed clinical improvement (radiological evaluation). Type II collagen induced arthritis is complement-dependent and is an example of an immune complex mediated injury. Thus, passive arthritis can be induced in rats by the intravenous administration of affinity-purified anticollagen IgG. The passive lesion is transient and the administered IgG is detected on the articular cartilage of the hind paws. This articular cartilage also contains complement C3. Passive arthritis is also complement-dependent. Suppression of Type II collagen arthritis can be induced by the prior intravenous treatment of rats with either Type II collagen or its constituent peptide α1, (II) CB10. Antigen-induced arthritis cannot be induced in those rats that have recovered from passive arthritis.
|Original language||English (US)|
|Number of pages||21|
|Journal||International Journal of Tissue Reactions|
|State||Published - Dec 1 1985|
ASJC Scopus subject areas
- Immunology and Allergy
- Cell Biology