Autoimmune reaction to type II collagen and cartilage degeneration in MRL/Mp- lpr/lpr mouse

• Published in: Rheumatology international Vol. 24; no. 2; pp. 84 - 92
• Main Authors: Tanaka, Maki, Fujii, Katsuyuki, Tsuji, Michiko, Sawai, Takashi
• Format: Journal Article
• Language: English
• Published: Germany Springer Nature B.V 01.03.2004
• Subjects: Animals; Arthritis; Arthritis, Rheumatoid - immunology; Autoantibodies - immunology; Autoimmune Diseases - complications; Autoimmune Diseases - immunology; Cartilage; Cartilage Diseases - complications; Cartilage Diseases - immunology; Collagen; Collagen Type II - immunology; Female; Mice; Mice, Inbred MRL lpr; Models, Animal
• ISSN: 0172-8172; 1437-160X
• DOI: 10.1007/s00296-003-0336-x

The early phase of cartilage degeneration was immunohistochemically examined in order to clarify the importance of autoimmune reaction against type II collagen in MRL/Mp- lpr/lpr (MRL/ l) mouse in an experimental model of rheumatoid arthritis (RA). Anti-type II collagen antibodies were detectable in 3-week-old mice and preceded the appearance of rheumatoid factors. Furthermore, mesenchymal cells and tartrate-resistant acid phosphatase-positive cells began to accumulate remarkably in the periphysis, a fibrochondro-osseous area in the bone marrow vicinity. The numbers of these cells increased with mice age, together with serum levels of anti-type II collagen antibodies. Immunostaining of the periphysis revealed expression of type II collagen, IgG, C3, Mac-3, MHC class II antigen Ia, and cathepsin-L. Osteoclast-like cells and macrophage infiltration into the lesion area were confirmed by transmission electron microscopy. The results indicate that cartilage degeneration in MRL/ l mouse may originate in the periphysis and progress via a pathway independent of synovial invasion.