HLA-B27 misfolding: a solution to the spondyloarthropathy conundrum?
Compelling evidence indicates that HLA-B27 is directly involved in the etiopathogenesis of the spondyloarthropathies (SpAs). Several hypotheses based on its native antigenic structure, the peptides it presents and mimicry with bacterial epitopes, have been proposed. However, these potential mechanisms remain largely unsupported by human studies and transgenic animal models. Recent work demonstrating that HLA-B27 misfolds offers a novel alternative hypothesis. Here, we review this new information on the folding and assembly of HLA-B27, and discuss consequences of misfolding that could be relevant to the pathogenesis of SpAs.
Colbert
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William S. Rowe Division of Rheumatology, Children's Hospital Medical Center, Cincinnati, OH 45229-3039, USA. bob.colbert@chmcc.org
D000818:Animals; D015796:HLA-B27 Antigen / Q000737:chemistry / Q000276:immunology*; D015395:Histocompatibility Antigens Class I / Q000235:genetics / Q000276:immunology; D006801:Humans; D011110:Polymorphism, Genetic; D017510:Protein Folding; D012216:Rheumatic Diseases / Q000276:immunology* / Q000628:therapy
D015796:HLA-B27 Antigen; D015395:Histocompatibility Antigens Class I