New aspects of spondyloarthritis pathogenesis. Part I. Genetic factors and role of HLA-B27 molecules
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Submission date: 2014-02-14
Acceptance date: 2014-03-12
Online publication date: 2014-06-04
Publication date: 2014-04-30
Reumatologia 2014;52(2):105–111
Recent data verify understanding of spondyloarthritis (SpA) pathogenesis by showing that there is the overlap between traditionally classified subtypes in terms of genetic background (HLA-B27 alleles, variants of IL-23R, ERAP1 and ERAP2 genes), which is discussed in this article. Moreover, there is also similarity in environmental factors and immunopathology, which will be the subject of next review articles. The view on the role of HLA-B27 molecules in SpA pathogenesis has also been changed. HLA-B27 molecules exist as canonical and non-canonical subtypes. The latter are formed by free heavy chains or heavy chain homodimers. Canonical HLA-B27 molecules present self and non-self antigens and thus initiate acquired immune response. By contrast, non-canonical HLA-B27 molecules trigger autoinflammatory response. This question is also discussed in this article.
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