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Understanding the Pathogenesis of Spondyloarthritis
Version 1
: Received: 13 July 2020 / Approved: 14 July 2020 / Online: 14 July 2020 (11:39:13 CEST)
How to cite: Sharip, A.; Kunz, J. Understanding the Pathogenesis of Spondyloarthritis. Preprints 2020, 2020070305. https://doi.org/10.20944/preprints202007.0305.v1 Sharip, A.; Kunz, J. Understanding the Pathogenesis of Spondyloarthritis. Preprints 2020, 2020070305. https://doi.org/10.20944/preprints202007.0305.v1
Abstract
Spondyloarthritis comprises of a group of inflammatory diseases of the joints and spine with various clinical manifestations. The group includes ankylosing spondylitis, reactive arthritis, psoriatic arthritis, arthritis associated with inflammatory bowel disease, and undifferentiated spondyloarthritis. The exact etiology and pathogenesis of spondyloarthritis are still unknown, but five hypotheses explaining the pathogenesis exist. These hypotheses suggest that spondyloarthritis is caused by arthritogenic peptides, an unfolded protein response, HLA-B27 homodimer formation, malfunctioning endoplasmic reticulum aminopeptidases, and, last but not least, gut inflammation and dysbiosis. Here we discuss the five hypotheses and the evidence supporting each. In all of these hypotheses, HLA-B27 plays a central role. It is likely that a combination of these hypotheses, with HLA-B27 taking center stage, will eventually explain the development of spondyloarthritis in predisposed individuals.
Keywords
spondyloarthritis; HLA-B27; pathogenesis; inflammation; arthritogenic peptides; unfolded protein response; ERAP1; gut dysbiosis
Subject
Biology and Life Sciences, Immunology and Microbiology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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