Complement activation by both classical and alternative pathways is critical for the effector phase of arthritis
(2004) In European Journal of Immunology 34(4). p.1208-1216- 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... (More)
- 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. (Less)
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https://lup.lub.lu.se/record/281654
- author
- Hietala, MA ; Nandakumar, KS ; Persson, L ; Fahlen, S ; Holmdahl, Rikard LU and Pekna, M
- organization
- publishing date
- 2004
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- rodent, complement, rheumatoid arthritis, transgenic, knockout
- in
- European Journal of Immunology
- volume
- 34
- issue
- 4
- pages
- 1208 - 1216
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- wos:000220834600032
- pmid:15048732
- scopus:3843142994
- ISSN
- 1521-4141
- DOI
- 10.1002/eji.200424895
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Medical Inflammation Research (013212019)
- id
- 79a17eb9-aa16-40a3-9a19-2c747190a333 (old id 281654)
- date added to LUP
- 2016-04-01 12:12:41
- date last changed
- 2022-01-27 00:27:28
@article{79a17eb9-aa16-40a3-9a19-2c747190a333,
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.}},
author = {{Hietala, MA and Nandakumar, KS and Persson, L and Fahlen, S and Holmdahl, Rikard and Pekna, M}},
issn = {{1521-4141}},
keywords = {{rodent; complement; rheumatoid arthritis; transgenic; knockout}},
language = {{eng}},
number = {{4}},
pages = {{1208--1216}},
publisher = {{John Wiley & Sons Inc.}},
series = {{European Journal of Immunology}},
title = {{Complement activation by both classical and alternative pathways is critical for the effector phase of arthritis}},
url = {{http://dx.doi.org/10.1002/eji.200424895}},
doi = {{10.1002/eji.200424895}},
volume = {{34}},
year = {{2004}},
}