Type IX collagen deficiency enhances the binding of cartilage-specific antibodies and arthritis severity 英文参考文献.docVIP

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Type IX collagen deficiency enhances the binding of cartilage-specific antibodies and arthritis severity 英文参考文献.doc

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Type IX collagen deficiency enhances the binding of cartilage-specific antibodies and arthritis severity 英文参考文献

Available online /content/8/4/R102 Research article Open Access Vol 8 No 4 Type IX collagen deficiency enhances the binding of cartilage-specific antibodies and arthritis severity Stefan Carlsen, Kutty Selva Nandakumar and Rikard Holmdahl Medical Inflammation Research, BMC I11, Lund University, SE-221 84 Lund, Sweden Corresponding author: Rikard Holmdahl, rikard.holmdahl@med.lu.se Received: 30 Mar 2006 Revisions requested: 10 May 2006 Revisions received: 26 May 2006 Accepted: 6 Jun 2006 Published: 3 Jul 2006 Arthritis Research Therapy 2006, 8:R102 (doi:10.1186/ar1989) This article is online at: /content/8/4/R102 ? 2006 Carlsen et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Joint cartilage is attacked in both autoimmune inflammatory and osteoarthritic processes. Type IX collagen (CIX) is a protein of importance for cartilage integrity and stability. In this study we have backcrossed a transgenic disruption of the col9a1 gene, which leads to an absence of CIX, into two different inbred mouse strains, DBA/1 and B10.Q. None of the CIX-deficient against type II collagen (CII) led to an earlier arthritis in the paws that also involved the knee joints. The antibodies used, which were specific for the J1 and the C1I epitopes of CII, initiate their arthritogenic attack by binding to cartilage. The C1I-specific antibodies bound to cartilage better in CIX-deficient mice than in wild-type animals, demonstrating that the lack of CIX in cartilage leads to an increased accessibility of structures for antibody binding and thus making the joints more vulnerable to inflammatory attack. These findings accentuate the importance of cartilage stability; cartilage disrupted as a result of ge