Systemic lupus erythematosus (SLE) is a genetically predisposed, female-predominant disease, characterized by multiple organ damage, that in its most severe forms can be life-threatening. The pathogenesis of SLE is complex and involves cells of both innate and adaptive immunity. The distinguishing feature of SLE is the production of autoantibodies, with the formation of immune complexes that precipitate at the vascular level, causing organ damage. Although progress in understanding the pathogenesis of SLE has been slower than in other rheumatic diseases, new knowledge has recently led to the development of effective targeted therapies, that hold out hope for personalized therapy. However, the new drugs available to date are still an adjunct to conventional therapy, which is known to be toxic in the short and long term. The purpose of this review is to summarize recent advances in understanding the pathogenesis of the disease and discuss the results obtained from the use of new targeted drugs, with a look at future therapies that may be used in the absence of the current standard of care or may even cure this serious systemic autoimmune disease.

T-helper 17 (Th17) cells represent a subpopulation of CD4+ T lymphocytes that play an essential role in defense against pathogens. Th17 cells are distinguished from Th1 and Th2 cells by their ability to produce members of the interleukin-17 (IL-17) family, namely IL-17A and IL-17F. IL-17 in turn induces several target cells to synthesize and release cytokines, chemokines, and metalloproteinases, thereby amplifying the inflammatory cascade. Th17 cells reside predominantly in the lamina propria of the mucosa. Their main physiological function is to maintain the integrity of the mucosal barrier against the aggression of infectious agents. However, in an appropriate inflammatory microenvironment, Th17 cells can transform into immunopathogenic cells, giving rise to inflammatory and autoimmune diseases. This review aims to analyze the complex mechanisms through which the interaction between Th17 and pathogens can be on the one hand favorable to the host by protecting it from infectious agents, and on the other hand harmful, potentially generating autoimmune reactions and tissue damage.

Purpose: To compare clinical features of uveitis in patients affected by psoriasis and psoriatic arthritis (PsA). Methods: A retrospective case-control study. Results: 117 patients were affected by uveitis and psoriasis or PsA (92 and 25 patients, respectively) from 2003 to 2013. Axial PsA was associated with unilateral uveitis onset compared to the peripheral pattern (p < 0.03). The prevalence of eyes with at least one complication involving anterior segment was significantly more represented in the PsA group than the psoriasis one (p = 0.024). Anterior segment complications were more frequently associated with posterior ones in PsA patients than in psoriasis patients (p = 0.005). Most common complications in total sample at baseline examination were cataract (29.7%), ocular hypertension (17%), macular edema (7%), and pupillary seclusion (4.4%). Conclusion: Uveitis in patients with psoriasis and PsA may have distinguishing clinical features. PsA patients have more ocular complications than those with psoriasis. Both groups need an ophthalmological examination to promptly detect ocular co-morbidity.

Purpose: To investigate clinical data, outcome, and treatment of intermediate uveitis in children. Methods: Retrospective cohort study, including 116 children affected by intermediate uveitis. Results: Sixty-two percent of patients were males. Ocular involvement was bilateral in 84%. Mean age at uveitis onset was 10.3 ± 3.6 years and 12.2 ± 7 years at first visit. Ninety-seven percent were classified as having idiopathic uveitis. The incidence of ocular complications during follow-up was 0.131/eye-year. Macular edema or a marked vitreous haze at presentation may be risks factors for incident visual loss. The most frequent causes of visual loss were macular edema (64%) and cataract (21%). Conclusions: Most cases are idiopathic (pars planitis); only few children presented associated systemic disease. Macular edema and severe vitritis at presentation are associated with increased risk of visual impairment. Cystoid macular edema is the main cause of visual impairment.

Background and Objectives: Interleukin-17 (IL-17) is a cytokine family consisting of six members and five specific receptors. IL-17A was the first member to be identified in 1993. Since then, several studies have elucidated that IL-17 has predominantly pro-inflammatory activity and that its production is involved in both the defense against pathogens and the genesis of autoimmune processes. Materials and Methods: In this review, we provide an overview of the role of interleukin-17 in the pathogenesis of juvenile idiopathic arthritis (JIA) and its relationship with IL-23, the so-called IL-23–IL-17 axis, by reporting updated findings from the scientific literature. Results: Strong evidence supports the role of interleukin-17A in the pathogenesis of JIA after the deregulated production of this interleukin by both T helper 17 (Th17) cells and cells of innate immunity. The blocking of IL-17A was found to improve the course of JIA, leading to the approval of the use of the human anti-IL17A monoclonal antibody secukinumab in the treatment of the JIA subtypes juvenile psoriatic arthritis (JPsA) and enthesitis-related arthritis (ERA). Conclusions: IL-17A plays a central role in the pathogenesis of JIA. Blocking its production with specific biologic drugs enables the effective treatment of this disabling childhood rheumatic disease.

Purpose: To describe the frequencies and risk factors of ocular complications and poor visual outcomes in children with juvenile idiopathic arthritis (JIA). Methods: Retrospective cohort study, including 69 consecutive children (116 eyes) affected by JIA-associated uveitis managed at a tertiary uveitis clinic. Results: The incidence of visual loss to the 20/50 or worse threshold was 0.04/eye-year (EY) and to the 20/200 or worse threshold was 0.02/EY. The most common complications at baseline were posterior synechiae (52%), band keratopathy (38%), and cataract (12%). Risk factor for a visual acuity threshold of 20/50 or worse included hypotony (p = 0.01; hazard ratio [HR] 3.7; 95% CI 1.3–10.4); anterior chamber flare >1 (p = 0.04; HR 1.3; 95% CI 0.5–3.4); a positive antinuclear antibody (ANA) (p = 0.02; HR1.4; 95% CI 0.8–2.4). Hypotony and positive ANA are also associated to the 20/200 or worse threshold (p = 0.03; HR 5.1; 95% CI 1.1–23.9 and p = 0.04; HR 1.0; 95% CI 0.4–2.3; respectively). Use of immunosuppressive drugs was associated with a reduced risk of visual loss of 20/200 or worse (odds ratio 0.14, 95% CI, 0.02–1.29; p = 0.04). Conclusions: Loss of vision and ocular complications still occur among children with JIA-related uveitis. Prompt diagnosis and a strict follow up associated to immunosuppressive therapy may decrease the poor visual outcome.