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Spondyloarthropathies

HLA-B27 and ERAP1 contribute to ankylosing spondylitis via aberrant peptide processing and presentation

Nature Reviews Rheumatology volume 7, page 498 (2011)Cite this article

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Protective allelic variants of ERAP1 displayed decreased rates of substrate trimming...

Ankylosing spondylitis (AS) is a highly heritable spondyloarthropathy that has been shown to be strongly associated with HLA-B27 variants, in addition to a number of other genetic loci, including IL23R, ERAP1, KIF21B, and the intergenic regions 2p15 and 21q22. A large, collaborative, genome-wide association study recently published in Nature Genetics has identified additional loci with strong associations with AS, and also provides insight into the mechanism by which HLA-B27 contributes to disease susceptibility and development.

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ORIGINAL RESEARCH PAPER

  1. Evans, D. M. et al. Interaction between ERAP1 and HLA-B27 in ankylosing spondylitis implicates peptide handling in the mechanism for HLA-B27 in disease susceptibility. Nat. Genet. doi:10.1038/ng.873

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  1. Nick Warde
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Warde, N. HLA-B27 and ERAP1 contribute to ankylosing spondylitis via aberrant peptide processing and presentation. Nat Rev Rheumatol 7, 498 (2011). https://doi.org/10.1038/nrrheum.2011.112

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  • DOI: https://doi.org/10.1038/nrrheum.2011.112

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