HLA class II and rheumatoid arthritis: the bumpy road of revelation

HLA class II and rheumatoid arthritis: the bumpy road of revelation Rheumatoid arthritis (RA) is a chronic auto-immune disease primarily targeting the joints. Approximately 1% of the population is affected by RA, and despite the improvements in therapeutic interventions, elucidation of the disease pathogenesis is still in its infancy. RA patients can be subdivided on basis of the presence of autoantibodies, especially anti-citrullinated protein antibodies (ACPA). ACPA+ and ACPA− disease most likely differ in aetiology, as different genetic and environmental risk factors are associated with these two disease entities. For ACPA+ RA disease, the genetic factors associating with disease mainly comprised of human leukocyte antigen (HLA) class II molecules. The predisposing HLA-DR alleles have been depicted as the ‘HLA Shared Epitope (SE) alleles’, as these alleles encode a similar sequence, the shared epitope sequence, within the beta chain of the HLA-DR molecule. In addition to the involvement of the HLA-SE alleles in the development of ACPA+ RA disease, other HLA-DR molecules have been shown to confer protection against this disease entity. The protective HLA molecules have, instead of the SE-motif, a different but shared sequence at the same location in the beta chain of HLA-DR molecules, consisting of the amino acid residues DERAA. The possible contributions of the predisposing and protective HLA molecules in association with ACPA-positive RA are discussed in this review. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Immunogenetics Springer Journals

HLA class II and rheumatoid arthritis: the bumpy road of revelation

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Publisher
Springer Berlin Heidelberg
Copyright
Copyright © 2017 by The Author(s)
Subject
Biomedicine; Immunology; Human Genetics; Gene Function; Cell Biology; Allergology
ISSN
0093-7711
eISSN
1432-1211
D.O.I.
10.1007/s00251-017-0987-5
Publisher site
See Article on Publisher Site

Abstract

Rheumatoid arthritis (RA) is a chronic auto-immune disease primarily targeting the joints. Approximately 1% of the population is affected by RA, and despite the improvements in therapeutic interventions, elucidation of the disease pathogenesis is still in its infancy. RA patients can be subdivided on basis of the presence of autoantibodies, especially anti-citrullinated protein antibodies (ACPA). ACPA+ and ACPA− disease most likely differ in aetiology, as different genetic and environmental risk factors are associated with these two disease entities. For ACPA+ RA disease, the genetic factors associating with disease mainly comprised of human leukocyte antigen (HLA) class II molecules. The predisposing HLA-DR alleles have been depicted as the ‘HLA Shared Epitope (SE) alleles’, as these alleles encode a similar sequence, the shared epitope sequence, within the beta chain of the HLA-DR molecule. In addition to the involvement of the HLA-SE alleles in the development of ACPA+ RA disease, other HLA-DR molecules have been shown to confer protection against this disease entity. The protective HLA molecules have, instead of the SE-motif, a different but shared sequence at the same location in the beta chain of HLA-DR molecules, consisting of the amino acid residues DERAA. The possible contributions of the predisposing and protective HLA molecules in association with ACPA-positive RA are discussed in this review.

Journal

ImmunogeneticsSpringer Journals

Published: Jul 11, 2017

References

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