Abstract
BackgroundUveitis is one of the most frequent ophthalmologic manifestations in rheumatology. Uveal inflammation can underlie a systemic inflammatory rheumatic disease (SIRD) in approximately 30% of cases with a significant burden on the quality of life since it represents a cause of blindness in up to 20% of cases in Western countries.MethodsIn this review, we provide a comprehensive overview of the pathophysiology of uveitis associated with SIRDs. According to our literature survey on the epidemiology of uveitis among SIRDs, spondyloarthritides, Behçet's disease and sarcoidosis get the major impact.ResultsIn Behçet's uveitis, the key players are highly polarized Th1 and Th17 lymphocytes, natural killer T cells and γδ T cells. All contribute to a great destructive inflammatory environment with the most serious visual damage resulting from the involvement of the posterior segment of the eye. In contrast, spondyloarthritides‐related uveitis derives from a complex interaction between genetic background and extra‐ocular inflammatory mediators originating from enthesitis, arthritis, psoriatic lesions and microbiome pro‐inflammatory alterations. In such conditions, the immune infiltration of CD4+ T cells, Th17 and natural killer cells along with pro‐inflammatory cytokines, TNF‐α among all, leads to intraocular inflammation. Lastly, granuloma formation represents the primary hallmark lesion in sarcoid uveitis. This suggests a profound link between the innate system that mainly recruits activated macrophages and adaptive system involving by Th1, Th17 and Th17.1 cells.ConclusionsAwareness among rheumatologists of a potential severe ocular involvement generates new insights into targeted therapeutic approaches and personalized treatments for each patient.
Highlights
In normal conditions, the eye is characterized by a privileged immune state, which is set to provide protection against local inflammation and to minimize the risk of visual impairment.[1]
This process is pronounced in systemic inflammatory rheumatic diseases (SIRDs), when effector leucocytes are already activated, the regulatory immune response is impaired and the damaged endothelium represents an entry gate for cytokines and inflammatory cells, eventually resulting in tissue damage through different mechanisms.[3,4]
An elevated expression of IL-17 receptor (IL- 17R) on CD8+ T cells in peripheral blood has been found in patients with ocular sarcoidosis compared with healthy controls suggesting a role of IL-17 signalling in sarcoidal ocular involvement[89] (Figure 3)
Summary
The eye is characterized by a privileged immune state, which is set to provide protection against local inflammation and to minimize the risk of visual impairment.[1]. Among the adaptive immune effectors in granulomas formation, Th17 cells display a key role, both in the classical variant of IL-17-s ecreting cells and through the Th17.1 phenotype which are IFN-γ-producing lymphocytes.[88] Interestingly, an elevated expression of IL-17 receptor (IL- 17R) on CD8+ T cells in peripheral blood has been found in patients with ocular sarcoidosis compared with healthy controls suggesting a role of IL-17 signalling in sarcoidal ocular involvement[89] (Figure 3). Studied to a lesser extent, the innate immune system plays its part in macrophage activation and granuloma formation: enhanced responses to TLR2 stimulation with induction of TNF-α have been detected in blood cells of patients with sarcoidosis.[91]. The latter are responsible for the maintenance of the granuloma through the synthesis of IFN-γ along with a qualitative deficiency of Tregs, incapable of curbing the uncontrolled immune reaction
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
