Project description:Experimental autoimmune uveitis (EAU) in Lewis rats is a model for the clinical heterogeneity of human uveitis. The autoantigens inducing disease in the rat are also seen in human disease. Depending upon the specific autoantigen used, the experimental disease course can be either monophasic or relapsing/remitting and appears to be dictated by the T cell effector phenotype elicited. We investigated potential differences between monophasic and relapsing/remitting effector T cells using transcriptomic profiling and pathway analysis. RNA samples isolated from three independent T cell lines derived from each specificity where analyzed by microarrays. Microarray data was used to obtain transcriptomic changes reflecting signal transduction pathway dysregulation. Keywords: Two group comparison Comparison of two types of cell lines of two different antigen specificities.
Project description:Experimental autoimmune uveitis (EAU) in Lewis rats is a model for the clinical heterogeneity of human uveitis. The autoantigens inducing disease in the rat are also seen in human disease. Depending upon the specific autoantigen used, the experimental disease course can be either monophasic or relapsing/remitting and appears to be dictated by the T cell effector phenotype elicited. We investigated potential differences between monophasic and relapsing/remitting effector T cells using transcriptomic profiling and pathway analysis. RNA samples isolated from three independent T cell lines derived from each specificity where analyzed by microarrays. Microarray data was used to obtain transcriptomic changes reflecting signal transduction pathway dysregulation. Keywords: Two group comparison
Project description:Retinal Müller glial cells (RMG) play a central role in retinal neuroinflammation, actively participating in the immune response and adopting a dynamic inflammatory phenotype. However, the precise functions of RMG in retinal inflammation remain incompletely understood. In this study, we investigated the proteome of RMG isolated from healthy horses and horses affected by equine recurrent uveitis (ERU). ERU serves as a unique spontaneous model of autoimmune uveitis, exhibiting key clinical and pathophysiological features observed in humans, such as a relapsing-remitting course of disease and a CD4+ T cell-driven autoimmune etiology [1, 2]. To gain insights into the molecular landscape of RMG in a spontaneous animal model of autoimmune uveitis and their potential contribution to retinal autoimmune neuroinflammation, we used discovery proteomics for the analysis of RMG from healthy horses and horses with ERU. Our data are not only relevant to veterinary medicine but also hold significant translational value for human ophthalmology as well. References: [1] Deeg, C.A., et al., Uveitis in horses induced by interphotoreceptor retinoid-binding protein is similar to the spontaneous disease. Eur J Immunol, 2002. 32(9): p. 2598-606. https://doi.org/10.1002/1521-4141(200209)32:9<2598::AID-IMMU2598>3.0.CO;2-%23 [2] Deeg, C.A., et al., CRALBP is a highly prevalent autoantigen for human autoimmune uveitis. Clin Dev Immunol, 2007. 2007: p. 39245. https://doi.org/10.1155/2007/39245
Project description:Uveitis is a severe autoimmune disease characereized by retinal inflammation, whicn brings harms to the visual function of the patients. We found that nimodipine could protect annimals from experimental autoimmune uveitis. To further clarify the possible mechanism through which nimodipine exerted effect, we performed genomic expression profiling of CD3+ T cells in EAU model and nimodipine treated group.
Project description:Autoimmune uveitis (AU) is a severe intraocular inflammatory disease driven by dysregulated T-cell immunity and macrophage activation, leading to retinal tissue damage. Experimental autoimmune uveitis (EAU), an animal model, closely mimics human AU, highlighting the role of macrophages in inflammation and immune regulation. Chronic sleep deprivation (CSD), caused by prolonged circadian rhythm disruption, further exacerbates immune dysfunction by activating microglia and enhancing inflammation. This study investigates the combined impact of EAU and CSD on retinal transcriptomics, focusing on immune and inflammatory pathways, providing insights into the interaction between circadian rhythm disruptions and autoimmune uveitis progression.
Project description:The gut microbiome influences the development of immune-mediated inflammatory diseases. One such condition is autoimmune uveitis, a sight-threatening ocular inflammation driven by retina-specific T cells. Using a model of spontaneous experimental autoimmune uveitis (sEAU) we showed that gut commensals provide immune stimuli that trigger the disease. Here we report that uveitis-promoting microbes are present in human gut flora and that colonization of germ-free (GF) mice with commensal flora from healthy human donors was sufficient to provoke disease. Severity of sEAU correlated with expansion of Akkermansia and contraction of short-chain fatty acid (SCFA)–producing Firmicutes, followed by decreased SCFA levels and a dominant gut Th1 effector response. Mechanistic gain-of-function experiments, enriching GF sEAU mice with Akkermansia, reproduced these microbiome, metabolite and immune phenotype shifts, and exacerbated disease. We propose that Akkermansia promotes autoimmunity by outcompeting SCFA-producers and enhancing Th1-type responses. Notably, an inverse correlation between Akkermansia (Verrucomicrobia) and Firmicutes was also present in fecal microbiome of patients with uveitis, multiple sclerosis and Crohn’s disease. These findings reveal a stereotypic gut microbial interaction network that regulates systemic immune balance, and may represent an ecologically conserved mechanism through which the gut microbiome modulates autoimmune and inflammatory diseases.
2026-08-03 | GSE327793 | GEO
Project description:The gut metagenome of experimental autoimmune uveitis mice
Project description:Uveitis is characterised by breakdown of the blood-retinal barrier (BRB), allowing infiltration of immune cells that mediate intraocular inflammation, which can lead to irreversible damage of the neuroretina and the loss of sight. Treatment of uveitis relies heavily on corticosteroids and systemic immunosuppression due to limited understanding of the molecular immune interactions that underpin ocular immune homeostasis. By performing single-cell transcriptomic analysis of whole dissociated mouse retinas with experimental autoimmune uveitis (EAU) versus healthy control, we gained an unbiased appreciation of the immune interactions that drive retinal inflammation in a model of posterior uveitis.
2024-08-29 | GSE241700 | GEO
Project description:Parental Uveitis Influences Offspring with an Increased Susceptibility to the Experimental Autoimmune Uveitis