Disease-associated polymorphisms in ERAP1 do not alter endoplasmic reticulum stress in patients with ankylosing spondylitis

TJ Kenna, MC Lau, P Keith, F Ciccia, ME Costello, Linda Bradbury, Poh-Lynn Low, Nitish Agrawal, Giovanni Triolo, Riccardo Alessandro, P. C. Robinson, Gethin Thomas, Matthew A. Brown

    Research output: Contribution to journalArticle

    24 Citations (Scopus)

    Abstract

    The mechanism by which human leukocyte antigen B27 (HLA-B27) contributes to ankylosing spondylitis (AS) remains unclear.Genetic studies demonstrate that association with and interaction between polymorphisms of endoplasmic reticulum aminopeptidase 1 (ERAP1) and HLA-B27 influence the risk of AS. It has been hypothesised that ERAP1-mediated HLA-B27 misfolding increases endoplasmic reticulum (ER) stress, driving an interleukin (IL) 23-dependent, pro-inflammatory immune response.We tested the hypothesis that AS-risk ERAP1 variants increase ER-stress and concomitant pro-inflammatory cytokine production inHLA-B27+ but not HLA-B27− AS patients or controls.
    Original languageEnglish
    Pages (from-to)35-42
    Number of pages8
    JournalGenes and Immunity
    Volume16
    Issue number1
    DOIs
    Publication statusPublished - 2015

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