Neutralization of IL-17 ameliorates uveitis but damages photoreceptors in a murine model of spondyloarthritis |
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| Authors: | Jelena M Kezic Tibor T Glant James T Rosenbaum Holly L Rosenzweig |
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| Affiliation: | (1) Casey Eye Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, Portland, OR 97239, USA;(2) JMK is now affiliated with Centre for Eye Research Australia, University of Melbourne, East Melbourne VIC, 3002, Australia;(3) Departments of Biochemistry and Orthopedics, Rush University Medical Center, 1735 W. Harrison St, Chicago, IL 60612, USA;(4) Department of Medicine, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, Portland, OR 97239, USA;(5) Department of Cell and Developmental Biology, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, Portland, OR 97239, USA;(6) Department of Molecular Microbiology and Immunology, Oregon Health & Science University, 3181 SW Sam Jackson Park Rd, Portland, OR 97239, USA;(7) Department of Anatomy and Developmental Biology, Monash University, Melbourne, VIC, Australia |
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| Abstract: | Introduction Uveitis, or intraocular inflammatory disease, is a frequent extra-articular manifestation of several forms of arthritis. Despite the frequent co-occurrence of uveitis and arthritis, little is understood of the eye's predisposition to this disease. We recently described a previously unreported uveitis in a murine model of spondyloarthropathy triggered by autoimmunity to aggrecan, a prominent proteoglycan (PG) macromolecule in cartilage. In contrast to the joint and spine, wherein interferon-gamma (IFNγ) deficiency reduced disease, IFNγ deficiency worsened uveitis. Given the regulatory role of IFNγ on the Th17 response and the current focus of anti-interleukin-17 therapeutics in patients with uveitis and spondyloarthritis, we sought to determine the extent to which interleukin (IL)-17 mediates uveitis in the absence of IFNγ. |
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