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Anti-citrullinated protein antibodies cause arthritis by cross-reactivity to joint cartilage
Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Southern Medical University, Guangzhou, China..
Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm,Southern Medical University, Guangzhou, China.
Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm.
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2017 (English)In: JCI insight, ISSN 2379-3708, Vol. 2, no 13, article id 93688Article in journal (Refereed) Published
Abstract [en]

Today, it is known that autoimmune diseases start a long time before clinical symptoms appear. Anti-citrullinated protein antibodies (ACPAs) appear many years before the clinical onset of rheumatoid arthritis (RA). However, it is still unclear if and how ACPAs are arthritogenic. To better understand the molecular basis of pathogenicity of ACPAs, we investigated autoantibodies reactive against the C1 epitope of collagen type II (CII) and its citrullinated variants. We found that these antibodies are commonly occurring in RA. A mAb (ACC1) against citrullinated C1 was found to cross-react with several noncitrullinated epitopes on native CII, causing proteoglycan depletion of cartilage and severe arthritis in mice. Structural studies by X-ray crystallography showed that such recognition is governed by a shared structural motif "RG-TG" within all the epitopes, including electrostatic potential-controlled citrulline specificity. Overall, we have demonstrated a molecular mechanism that explains how ACPAs trigger arthritis.

Place, publisher, year, edition, pages
2017. Vol. 2, no 13, article id 93688
National Category
Rheumatology and Autoimmunity
Identifiers
URN: urn:nbn:se:liu:diva-144204DOI: 10.1172/jci.insight.93688PubMedID: 28679953OAI: oai:DiVA.org:liu-144204DiVA, id: diva2:1172628
Available from: 2018-01-10 Created: 2018-01-10 Last updated: 2018-05-04

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Skogh, ThomasKastbom, Alf
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Division of Neuro and Inflammation ScienceFaculty of Medicine and Health SciencesDepartment of Rheumatology
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