Role of MHC Genes and T Cell Receptor Genes in Collagen Induced Arthritis in Mice
Type II collagen induced arthritis (CIA) is an experimental model of autoimmune inflammatory polyarthritis sharing certain similarities with human rheumatoid arthritis (1). It is characterized by redness, swelling and deformity (Fig. 1) in the peripheral joints, following a latent period varying from 3 to 8 weeks after intradermal immunization with native type II collagen (from homologous or heterologous species) in adjuvant. The disease has been described in rats (2), mice (3), and in primates (4). Type II collagen is a “sequestered” antigen present in only a few sites in the body including hyaline cartilage, ears, and vitreous humor of the eye (5). An autoimmune reaction to the type II collagen present in hyaline cartilage of peripheral joints is thought to be the primary etiologic factor in the disease process. Histologically (5), the disease is characterized by the initial deposition of fibrin, followed by infiltration of the synovium with mononuclear and polymorphonuclear cells with synovial hyperplasia and pannus formation (Fig. 2). Cartilage and bone erosions then follow progressing onto the total destruction of the joint with deposition of fibrous tissue and subsequent ankylosis. The acute phase of the disease is thought to be initiated by the deposition of pathogenic anti-type II collagen antibodies on the cartilage followed by activation and deposition of complement in the affected joints, as shown by immunofluorescence (6). Animals depleted of complement fail to develop the disease (7).
KeywordsCollagen Induce Arthritis Collagen Molecule Cyanogen Bromide Cell Receptor Gene Versus Gene Segment
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