Disease relevance of Uveitis

• We analyzed data from renal biopsies performed in 192 patients (129 adults and 63 children) who had been treated with cyclosporine for insulin-dependent diabetes mellitus of recent onset, uveitis, psoriasis, Sjögren's syndrome, or polychondritis [1].
• Interleukin 12 protects from a T helper type 1-mediated autoimmune disease, experimental autoimmune uveitis, through a mechanism involving interferon gamma, nitric oxide, and apoptosis [2].
• Arthritis, uveitis, and Stevens-Johnson syndrome induced by trimethoprim [3].
• Some of these clinical features are shared by more common, potentially blinding, conditions including diabetic retinopathy, uveitis, and retinitis pigmentosa [4].
• A double-blind, placebo-controlled, phase III multi-center trial of oral myelin in 515 relapsing-remitting multiple sclerosis patients is in progress, as are phase II clinical trials investigating the oral administration of type II collagen in rheumatoid arthritis, S-antigen in uveitis, and insulin in type I diabetes [5].

Psychiatry related information on Uveitis

• We have studied 44 sera of patients with uveitis, and controls for the presence of ANF and other antinuclear antibodies (ss-DNA, ds-DNA, Poly (I), Poly (G), RNP, Sm, histones) and for the presence of a common anti-DNA idiotype (16/6 Id) employing the ELISA method [6].

High impact information on Uveitis

• There were fewer episodes of hypopyon uveitis (1 vs. 15; P less than 0.001) among the group 2 patients who took azathioprine [7].
• Saving the vision of children with juvenile rheumatoid arthritis-associated uveitis [8].
• Bilateral uveitis was the initial manifestation of a limited form of Wegener granulomatosis in a 47-year-old man [9].
• Susceptibility to experimental autoimmune uveitis (EAU), a model for human uveitis induced in mice with the retinal antigen interphotoreceptor retinoid-binding protein (IRBP), is controlled by "natural" CD4(+)CD25(+) regulatory T (T reg) cells [10].
• Experimental autoimmune uveitis (EAU) is a disease of the neural retina induced by immunization with retinal antigens, such as interphotoreceptor retinoid-binding protein (IRBP) and arrestin (retinal soluble antigen, S-Ag) [11].

Chemical compound and disease context of Uveitis

• Renal histopathologic alterations in patients treated with cyclosporine for uveitis [12].
• Cyclosporin a. Inhibition of experimental autoimmune uveitis in Lewis rats [13].
• Rescue therapy with mycophenolate mofetil in refractory uveitis [14].
• Hypotensive effect of timolol on secondary glaucoma in chronic uveitis [15].
• Treatment of chronic endogenous uveitis with fusidic acid [16].
• Overall, there were 43 cases of uveitis associated with etanercept, 14 associated with infliximab, and 2 associated with adalimumab [17].

Biological context of Uveitis

• The retinal autoantigens S-antigen (S-Ag) and interphotoreceptor retinoid binding protein (IRBP) can induce autoimmune uveitis in rodent models [18].
• Here, we have analyzed the T cell repertoire at the autoimmune site by examining V beta gene expression in the retinas of rats with SAg- or IRBP-induced uveitis [19].
• Kinetics of intraocular tumor necrosis factor and interleukin-6 in endotoxin-induced uveitis in the rat [20].
• Long-term cytogenetic follow-up study of patients with uveitis treated with chlorambucil [21].
• We have studied the long-term effects of chlorambucil treatment on the chromosomes of peripheral blood lymphocytes from patients with uveitis [21].

Anatomical context of Uveitis

• In a model of low-dose endotoxin-induced uveitis, anti-LOX-1 antibody efficiently suppressed leukocyte infiltration and protein exudation [22].
• Autoimmune encephalomyelitis and uveitis induced by T cell immunity to self beta-synuclein [23].
• We show here that ocular lymphocytes isolated from patients with uveitis who had been treated with topical glucocorticoids expressed highly elevated levels of CXCR4 [24].
• In addition, the induced CD56(bright) cells could secrete large amounts of IL-10 whereas CD56(dim) NK cells could not, suggesting that the induction of the CD56(bright) cells may have a beneficial effect on the remission of active uveitis [25].
• The severity of uveitis was evaluated clinically at 16 hours, and nitrite levels were evaluated in the aqueous humor at 8 hours [26].

Gene context of Uveitis

• Untreated uveitis and noninflammatory AqH up-regulated CXCR4 to a limited extent; this was dependent on TGF-beta2 [24].
• Taken together, our data suggest that ongoing CD40/CD40L blockade might be required to maintain a therapeutic effect against uveitis [27].
• Inhibition of endotoxin-induced uveitis and potentiation of local TNF-alpha and interleukin-6 mRNA expression by interleukin-13 [28].
• CONCLUSIONS: Various immunoregulatory cytokines (IL-6, IL-10, and IFN-gamma) were detected in ocular fluid samples from patients with uveitis [29].
• Interleukin-10 was reduced (p = 0.024) in uveitis in comparison with controls [30].

Analytical, diagnostic and therapeutic context of Uveitis

• We used this principle to design a strategy for gene therapy of experimental autoimmune uveitis, a cell-mediated autoimmune disease model for human uveitis induced with the uveitogenic interphotoreceptor retinoid-binding protein (IRBP) [31].
• To determine whether CD40L blockade resulted in long-term tolerance, mice protected by treatment with MR1 Ab were rechallenged for uveitis after circulating MR1 Ab levels dropped below the detection limit of ELISA [27].
• The results obtained in experimental animal models have led to the conduction of several clinical trials of oral tolerance in patients with multiple sclerosis, rheumatoid arthritis, uveitis, and IDDM [32].
• The ability to suppress disease experimentally has led to the successful translation of anti-TNF therapy for treatment of uveitis in cohort studies and phase I/II trials where, additionally, altered peripheral blood CD4(+) T-cell profiles can be demonstrated following each treatment [33].
• S-antigen induces autoimmune uveitis in the animal model and is a major autoantigen in human disease [34].

References