Ankylosing spondylitis: an autoimmune or autoinflammatory disease?

Daniele Mauro, Ranjeny Thomas, Giuliana Guggino, Rik Lories, Matthew A. Brown, Francesco Ciccia*

*Corresponding author for this work

    Research output: Contribution to journalReview articlepeer-review

    121 Citations (Scopus)

    Abstract

    Ankylosing spondylitis (AS) is a chronic inflammatory disorder of unknown aetiology. Unlike other systemic autoimmune diseases, in AS, the innate immune system has a dominant role characterized by aberrant activity of innate and innate-like immune cells, including γδ T cells, group 3 innate lymphoid cells, neutrophils, mucosal-associated invariant T cells and mast cells, at sites predisposed to the disease. The intestine is involved in disease manifestations, as it is at the forefront of the interaction between the mucosal-associated immune cells and the intestinal microbiota. Similarly, biomechanical factors, such as entheseal micro-trauma, might also be involved in the pathogenesis of the articular manifestation of AS, and sentinel immune cells located in the entheses could provide links between local damage, genetic predisposition and the development of chronic inflammation. Although these elements might support the autoinflammatory nature of AS, studies demonstrating the presence of autoantibodies (such as anti-CD74, anti-sclerostin and anti-noggin antibodies) and evidence of activation and clonal expansion of T cell populations support an autoimmune component to the disease. This Review presents the evidence for autoinflammation and the evidence for autoimmunity in AS and, by discussing the pathophysiological factors associated with each, aims to reconcile the two hypotheses.

    Original languageEnglish
    Pages (from-to)387-404
    Number of pages18
    JournalNature Reviews Rheumatology
    Volume17
    Issue number7
    DOIs
    Publication statusPublished - Jul 2021

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