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Structure and pathogenicity of antibodies specific for citrullinated collagen type II in experimental arthritis
Lund University, Lund, Sweden; Karolinska Institutet, Stockholm, Sweden.
Lund University, Lund, Sweden.
Lund University, Lund, Sweden; Karolinska Institutet, Stockholm, Sweden.ORCID iD: 0000-0001-7790-8197
Friedrich-Alexander-University of Erlangen-Nuremberg, Erlangen, Germany.
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2009 (English)In: Journal of Experimental Medicine, ISSN 0022-1007, E-ISSN 1540-9538, Vol. 206, no 2, p. 449-62Article in journal (Refereed) Published
Abstract [en]

Antibodies to citrulline-modified proteins have a high diagnostic value in rheumatoid arthritis (RA). However, their biological role in disease development is still unclear. To obtain insight into this question, a panel of mouse monoclonal antibodies was generated against a major triple helical collagen type II (CII) epitope (position 359-369; ARGLTGRPGDA) with or without arginines modified by citrullination. These antibodies bind cartilage and synovial tissue, and mediate arthritis in mice. Detection of citrullinated CII from RA patients' synovial fluid demonstrates that cartilage-derived CII is indeed citrullinated in vivo. The structure determination of a Fab fragment of one of these antibodies in complex with a citrullinated peptide showed a surprising beta-turn conformation of the peptide and provided information on citrulline recognition. Based on these findings, we propose that autoimmunity to CII, leading to the production of antibodies specific for both native and citrullinated CII, is an important pathogenic factor in the development of RA.

Place, publisher, year, edition, pages
New York, NY: Rockefeller University Press, 2009. Vol. 206, no 2, p. 449-62
National Category
Immunology in the medical area
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URN: urn:nbn:se:hh:diva-48852DOI: 10.1084/jem.20081862ISI: 000266008800017PubMedID: 19204106Scopus ID: 2-s2.0-63049101247OAI: oai:DiVA.org:hh-48852DiVA, id: diva2:1719020
Note

Funding text: This work was supported by the Swedish Research Council, the Strategic Science Foundation, the Research School inPharmaceutical Sciences at Lund University, the Crafoord Foundation, the Kock Foundation, the Osterlunds Foundation, the Alex and Eva Wallstrom Foundation, the European Union Grants Autocure (grant LSHB-2006-018661), MUGEN (grant LSHG-CT-2005-005203), and the Doktor Robert Pfleger Foundation (grant to H. Burkhardt).

Available from: 2022-12-14 Created: 2022-12-14 Last updated: 2023-02-21Bibliographically approved

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Nandakumar, Kutty Selva

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