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Complement deficiency ameliorates collagen-induced arthritis in mice.
Max Albert Hietala1, Ing-Marie Jonsson, Andrej Tarkowski
1Department of Medical Biochemistry, Göteborg University, Göteborg, Sweden.
Journal of Immunology (Baltimore, Md. : 1950)
|June 22, 2002
Summary
The complement system plays a harmful role in collagen-induced arthritis (CIA). Complement-deficient mice showed resistance to CIA, indicating complement activation contributes to rheumatoid arthritis development.
Area of Science:
- Immunology
- Rheumatology
- Animal Models
Background:
- Collagen-induced arthritis (CIA) models human rheumatoid arthritis, involving synovitis and joint destruction.
- The complement system's role in CIA pathogenesis remains incompletely understood.
Purpose of the Study:
- To investigate the involvement of complement factors C3 and factor B in CIA.
- To elucidate the contribution of classical and alternative complement pathways to arthritis development.
Main Methods:
- DBA/1J mice deficient in complement factor C3 (C3(-/-)) and factor B (FB(-/-)) were used.
- Mice were immunized with bovine collagen type II to induce CIA.
- Arthritis severity and collagen type II-specific IgG antibody titers were measured.
Main Results:
- Control mice developed severe CIA and high antibody titers.
- C3(-/-) and FB(-/-) mice were resistant to CIA and showed reduced antibody responses.
- Re-immunization triggered arthritis in complement-deficient mice, with C3(-/-) showing mild and FB(-/-) intermediate severity.
Conclusions:
- Complement activation via both classical and alternative pathways is detrimental in CIA.
- Targeting complement pathways may offer therapeutic strategies for rheumatoid arthritis.