Linked Life Data

16849503

Source:http://linkedlifedata.com/resource/pubmed/id/16849503

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2006-7-19
pubmed:abstractText
Activation of each complement initiation pathway (classical, alternative, and lectin) can lead to the generation of bioactive fragments with resulting inflammation in target organs. The objective of the current study was to determine the role of specific complement activation pathways in the pathogenesis of experimental anti-type II collagen mAb-passive transfer arthritis. C57BL/6 mice were used that were genetically deficient in either the alternative pathway protein factor B (Bf(-/-)) or in the classical pathway component C4 (C4(-/-)). Clinical disease activity was markedly decreased in Bf(-/-) compared with wild-type (WT) mice (0.5 +/- 0.22 (n = 6) in Bf(-/-) vs 8.83 +/- 0.41 (n = 6) in WT mice (p < 0.0001)). Disease activity scores were not different between C4(-/-) and WT mice. Analyses of joints showed that C3 deposition, inflammation, pannus, cartilage, and bone damage scores were all significantly less in Bf(-/-) as compared with WT mice. There were significant decreases in mRNA levels of C3, C4, CR2, CR3, C3aR, and C5aR in the knees of Bf(-/-) as compared with C4(-/-) and WT mice with arthritis; mRNA levels for complement regulatory proteins did not differ between the three strains. These results indicate that the alternative pathway is absolutely required for the induction of arthritis following injection of anti-collagen Abs. The mechanisms by which these target organ-specific mAbs bypass the requirements for engagement of the classical pathway remain to be defined but do not appear to involve a lack of alternative pathway regulatory proteins.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
177
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1904-12
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16849503-Animals, pubmed-meshheading:16849503-Antibodies, Monoclonal, pubmed-meshheading:16849503-Arthritis, Experimental, pubmed-meshheading:16849503-Cartilage, Articular, pubmed-meshheading:16849503-Collagen, pubmed-meshheading:16849503-Complement C3, pubmed-meshheading:16849503-Complement C4, pubmed-meshheading:16849503-Complement Factor B, pubmed-meshheading:16849503-Complement Factor H, pubmed-meshheading:16849503-Complement Inactivator Proteins, pubmed-meshheading:16849503-Complement Pathway, Alternative, pubmed-meshheading:16849503-Cytokines, pubmed-meshheading:16849503-Disease Models, Animal, pubmed-meshheading:16849503-Immunization, Passive, pubmed-meshheading:16849503-Immunohistochemistry, pubmed-meshheading:16849503-Inflammation, pubmed-meshheading:16849503-Male, pubmed-meshheading:16849503-Mice, pubmed-meshheading:16849503-Mice, Inbred C57BL, pubmed-meshheading:16849503-Mice, Knockout, pubmed-meshheading:16849503-RNA, Messenger, pubmed-meshheading:16849503-Synovial Membrane
pubmed:year
2006
pubmed:articleTitle
Alternative complement pathway activation is essential for inflammation and joint destruction in the passive transfer model of collagen-induced arthritis.
pubmed:affiliation
Divisions of Rheumatology, University of Colorado Health Sciences Center, Denver, CO 80262, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural