Comparison of clinical and experimental uveitis

Abstract

Uveitis is a term which encompasses many clinical syndromes which would appear to be discrete entities. Both clinically and experimentally, the separation of uveitis affecting only the anterior segment from that affecting the posterior segment has a sound pathogenetic basis. However, clear distinctions among the various forms of endogenous posterior uveitis are more difficult to maintain in the light of evidence from experimental models of autoimmune uveitis (EAU). EAU can be induced by a variety of retinal antigens and each antigen has been shown to induce somewhat different forms of EAU, depending on such factors as dose of antigen, species and strains of animal model, and the type(s) of adjuvant used. However, within each model a similar spectrum of uveoretinal responses can be induced by each antigen suggesting that the pathogenetic mechanisms are probably similar also. In addition, if these models are analogous to human disease, then each clinical entity within this apparently heterogeneous group of clinical posterior uveitis syndromes may represent one aspect of a general organ-specific uveoretinal response to autoantigens.

Anti-inflammatory treatment of uveitis with biologicals: new treatment options that reflect pathogenetic knowledge of the disease

“…Experimental autoimmune uveitis (EAU), which can be induced in mice and rats by immunization with ocular proteins in adjuvants, serves as a model of human autoimmune uveitis [13]. While EAU in mice can only be induced with IRBP or an IRBP-derived peptide, a variety of retinal autoantigens and their peptides are pathogenic in rats.…”

Soluble intercellular adhesion molecule-1 (sICAM-1) as a marker of disease relapse in idiopathic uveoretinitis

“…Although the evidence for idiopathic uveitis being an organspecific autoimmune disease is weak (based primarily on the existence of an animal model (experimental allergic uveoretinitis) with similar histopathological features to the human disease [3]), most would agree that immune responses play the principal if not the primary role in pathogenesis [4]. In the clinical management of uveitis, histological examination of intraocular inflammation is rarely possible for technical and ethical reasons, and peripheral blood changes remain the only practical method of monitoring disease activity and more importantly of predicting disease relapse.…”

Inhibition of tumor necrosis factor activity minimizes target organ damage in experimental autoimmune uveoretinitis despite quantitatively normal activated T cell traffic to the retina

“…To resolve this issue, we have turned to experimental autoimmune uveoretinitis (EAU) , an established model of human posterior uveitis [18]. EAU is induced by immunization with retinal antigens including a heterologous mixture of soluble retinal antigens derived from the rod outer segments (ROS) or transfer of retinal antigenspecific CD4' T cells .…”