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Autoimmunity in rheumatoid arthritis (RA) is characterized by an antibody response to citrullinated proteins. Two of the risk factors for RA-HLA-DRB1 shared epitope alleles and smoking-are also associated with periodontitis, which is largely, but not exclusively, caused by Porphyromonas gingivalis infection. Furthermore, RA and periodontitis have a similar pathophysiology, characterized by destructive inflammation. The citrullination of proteins by P. gingivalis and the subsequent generation of autoantigens that drive autoimmunity in RA represents a possible causative link between these two diseases. Antibodies directed towards the immunodominant epitope of human citrullinated α-enolase cross-react with a conserved sequence on citrullinated P. gingivalis enolase. On the basis of this cross-reactivity, in this Perspectives article we explore the hypothesis of molecular mimicry in the etiology of RA, with citrullinated enolase as the specific antigen involved.

Original publication

DOI

10.1038/nrrheum.2010.139

Type

Journal article

Journal

Nat Rev Rheumatol

Publication Date

12/2010

Volume

6

Pages

727 - 730

Keywords

Arthritis, Rheumatoid, Autoimmunity, Bacteroidaceae Infections, Citrulline, Humans, Periodontitis, Phosphopyruvate Hydratase, Porphyromonas gingivalis, Risk Factors