REVIEW PAPER
New aspects of spondyloarthritis pathogenesis. Part I. Genetic factors and role of HLA-B27 molecules
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
KEYWORDS
TOPICS
ABSTRACT
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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Copyright: © Narodowy Instytut Geriatrii, Reumatologii i Rehabilitacji w Warszawie. This is an Open Access journal, all articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (https://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
| eISSN: | 2084-9834 |
| ISSN: | 0034-6233 |
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