| First Author | Hietala MA | Year | 2004 |
| Journal | Eur J Immunol | Volume | 34 |
| Issue | 4 | Pages | 1208-16 |
| PubMed ID | 15048732 | Mgi Jnum | J:88872 |
| Mgi Id | MGI:3037378 | Doi | 10.1002/eji.200424895 |
| Citation | Hietala MA, et al. (2004) Complement activation by both classical and alternative pathways is critical for the effector phase of arthritis. Eur J Immunol 34(4):1208-16 |
| abstractText | To analyze the role of the classical and alternative pathways of complement activation in the effector phase of arthritis, we have induced arthritis in C3- and factor B (FB)-deficient (C3(-/-) and FB(-/-)) DBA/1J mice using well-defined monoclonal IgG2b and IgG2a antibodies to type II collagen. In control DBA/1J mice, severe swelling of the joints, destruction of cartilage and erosion of bone developed very rapidly with a 100% incidence and a peak on days 7-10. Although 75% of C3(-/-) mice developed arthritis, the clinical severity was very mild and the onset was delayed. Severity of arthritis in FB(-/-) mice ranked intermediate in comparison with C3(-/-) and control mice with an incidence of 100%. Immunohistochemical analysis of the inflamed joints demonstrated substantial reduction in macrophage and neutrophilic leukocyte infiltration in both C3(-/-) and FB(-/-) mice, thereby confirming the clinical findings. We conclude that both the classical and the alternative pathways of complement activation are involved in the effector phase of arthritis. |
