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  • Review Article
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The eye: a window of opportunity in rheumatoid arthritis?

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Key Points

  • Rheumatoid arthritis (RA) is associated with severe ocular surface complications such as scleritis

  • RA is the most common autoimmune disease associated with dry eye syndrome

  • The immunological landscape of the eye has much in common with that of the joint in RA; the eye is accessible to noninvasive techniques for monitoring the changes in the immune system in RA

  • Innate and adaptive defences of the eye and the joint are disturbed in RA, which can result in different clinical manifestations of ocular surface inflammation

  • Systemic treatment of RA counteracts ocular complications; topical, targeted treatment of ocular surface inflammation with less toxicity could be possible for RA

Abstract

Rheumatoid arthritis (RA), the most common autoimmune disorder associated with dry eye syndrome, is also associated with sight-threatening ocular diseases such as peripheral ulcerative keratitis, scleritis and corneal melts. Tissue damage on the ocular surface of patients with RA is autoimmune-mediated. Findings from patients with dry eye have implicated defects in innate immunity (Toll-like receptors, S100A and resident antigen-presenting cells), cytokines, chemokines and T helper (TH)-cell subsets (including TH1 and TH17) in disease pathogenesis. Some of these features are probably important in dry eye related to RA, which can occur at a different time from articular disease and is more clinically severe than idiopathic dry eye. Ocular surface immune factors can be influenced by the systemic immune landscape. Depending on the severity of ocular inflammation in RA, treatment can include ciclosporin, topical corticosteroids, tacrolimus, autologous serum and systemic immunosuppression. Tissue damage is treated by inhibiting matrix metalloproteinases. Potential therapeutic strategies benefit from an improved understanding of ocular surface immunology, and include targeting of T-cell subsets, B-cell signalling or cytokines.

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Figure 1: TH17 cell polarisation in RA-associated ocular surface inflammation.
Figure 2: Pathogenesis of ocular surface inflammation in RA.

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Change history

  • 25 June 2014

    In the version of this article initially published online, the name of author York Kiat Tan was misspelled. The error has been corrected for the HTML, PDF and print versions of the article.

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Acknowledgements

L.T. is supported by the Singapore National Research Foundation under its clinician scientist award NMRC/CSA/045/2012 and administered by the Singapore Ministry of Health's National Medical Research Council, and by the Singapore Biomedical Research Council BMRC 10/1/35/19/670. S.A. is supported by the NMRC Singapore Translational Research (STAR) Award NMRC/STaR/020/2013, Duke-National University of Singapore and Singapore Health Services.

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L.T. researched data for the article. All authors made equal contribution to substantial discussion of content, writing and reviewing/editing the manuscript before submission.

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Correspondence to Louis Tong.

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Tong, L., Thumboo, J., Tan, Y. et al. The eye: a window of opportunity in rheumatoid arthritis?. Nat Rev Rheumatol 10, 552–560 (2014). https://doi.org/10.1038/nrrheum.2014.85

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