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Rheumatology Advance Access originally published online on March 3, 2008
Rheumatology 2008 47(5):567-571; doi:10.1093/rheumatology/ken014
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

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Consequence of neo-antigenicity of the ‘altered self’

P. Eggleton1, R. Haigh1,2 and P. G. Winyard1

1Musculoskeletal and Inflammation Research Group, Institute of Biomedical and Clinical Science, Peninsula College of Medicine and Dentistry, Universities of Exeter and Plymouth and 2Princess Elizabeth Orthopaedic Centre, Exeter, UK.

Correspondence to: P. G. Winyard, Peninsula College of Medicine and Dentistry, St Luke's Campus, Universities of Exeter and Plymouth, Exeter, Devon EX1 2LU, UK. E-mail: paul.winyard{at}pms.ac.uk


  Abstract

Post-translational modifications play a central role in determining the function of proteins. Such protein modifications come in a great variety of guises, and include phosphorylation, proteolysis, glycosylation, citrullination and oxidative modifications. In relation to inflammatory autoimmune diseases, some post-translational modifications appear to result in the generation of new antigens, and hence autoantibodies. Examples include: the induction of peptide immunogenicity by the spontaneous conversion of aspartic acid residues to isoaspartic acid; granzyme B-mediated cleavage of SLE autoantigens; the oxidative modification—on the surface of apoptotic cells—of lipids and proteins, rendering them immunogenic; and the presence of antibodies to oxidatively modified type II collagen and C1q in RA and SLE patients, respectively. The measurement of autoantibodies to citrullinated proteins has been verified as a very useful diagnostic tool in RA. Proteomics techniques, in principle, allow the detection of all types of in vivo protein modifications, and the increasing application of such technologies to the study of rheumatological diseases will further our understanding of autoantigenicity.

KEY WORDS: Post-translational modification, Protein oxidation, Citrullination, Oxidized low-density lipoprotein, Inflammation, Rheumatic diseases, Anti-phospholipid syndrome, Neo-antigenicity, Autoantibody, Apoptosis

Submitted 7 September 2007; revised version accepted 7 January 2008.
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