Specific interaction between genotype, smoking and autoimmunity to citrullinated α-enolase in the etiology of rheumatoid arthritis-Reference-Cited by-同舟云学术

Specific interaction between genotype, smoking and autoimmunity to citrullinated α-enolase in the etiology of rheumatoid arthritis

Published:2009-11-08 Issue:12 Volume:41 Page:1319-1324
ISSN:1061-4036
Container-title:Nature Genetics
language:en
Short-container-title:Nat Genet

Author:

Mahdi Hiba,Fisher Benjamin A,Källberg Henrik,Plant Darren,Malmström Vivianne,Rönnelid Johan,Charles Peter,Ding Bo,Alfredsson Lars,Padyukov Leonid,Symmons Deborah P M,Venables Patrick J,Klareskog Lars,Lundberg Karin

Publisher

Springer Science and Business Media LLC

Subject

Genetics

Link

http://www.nature.com/articles/ng.480.pdf

Reference34 articles.

1. Klareskog, L. et al. A new model for an etiology of rheumatoid arthritis: smoking may trigger HLA-DR (shared epitope)-restricted immune reactions to autoantigens modified by citrullination. Arthritis Rheum. 54, 38–46 (2006).

2. Huizinga, T.W. et al. Refining the complex rheumatoid arthritis phenotype based on specificity of the HLA-DRB1 shared epitope for antibodies to citrullinated proteins. Arthritis Rheum. 52, 3433–3438 (2005).

3. Kinloch, A. et al. Identification of citrullinated alpha-enolase as a candidate autoantigen in rheumatoid arthritis. Arthritis Res. Ther. 7, R1421–R1429 (2005).

4. Lundberg, K. et al. Antibodies to citrullinated alpha-enolase peptide 1 are specific for rheumatoid arthritis and cross-react with bacterial enolase. Arthritis Rheum. 58, 3009–3019 (2008).

5. Gregersen, P.K., Silver, J. & Winchester, R.J. The shared epitope hypothesis. An approach to understanding the molecular genetics of susceptibility to rheumatoid arthritis. Arthritis Rheum. 30, 1205–1213 (1987).

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