Complement activation by both classical and alternative pathways is critical for the effector phase of arthritis |
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Authors: | Hietala Max Albert Nandakumar Kutty S Persson Linda Fahlén Susann Holmdahl Rikard Pekna Marcela |
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Affiliation: | Department of Medical Biochemistry, G?teborg University, G?teborg, Sweden. |
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Abstract: | 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. |
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Keywords: | Complement Rheumatoid arthritis Rodent Transgenic/knockout |
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