HLA-B27 misfolding: a solution to the spondyloarthropathy conundrum?

Mol Med Today. 2000 Jun;6(6):224-30. doi: 10.1016/s1357-4310(00)01699-3.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • HLA-B27 Antigen / chemistry
  • HLA-B27 Antigen / immunology*
  • Histocompatibility Antigens Class I / genetics
  • Histocompatibility Antigens Class I / immunology
  • Humans
  • Polymorphism, Genetic
  • Protein Folding*
  • Rheumatic Diseases / immunology*
  • Rheumatic Diseases / therapy


  • HLA-B27 Antigen
  • Histocompatibility Antigens Class I