Autoimmune diseases of the eye
Abstract: In recent years considerable headway has been made on understanding the mechanisms underlying inflammatory diseases of the eye. This includes the role of the innate vs. adaptive arms of the immune systems in disease, the concept that distinct immune pathways can drive end-organ pathology, and the role as well as limitations of immune privilege in controlling the innate and adaptive effector responses that lead to eye pathology and loss of vision. These insights have largely been derived from basic studies in established and in newly developed animal models of uveitis. The increased understanding of disease mechanisms has the potential to guide development of rational therapies for human uveitis. Many novel biologics currently in use or being evaluated have been developed, or validated, in animal models of autoimmune and inflammatory disease, including experimental uveitis. Paradoxically, and fueled in part by dwindling research budgets, a campaign has been gathering momentum against use of animal models in preclinical research, as being poorly representative of responses in humans. Given the extensive genetic similarity between humans and laboratory rodents as revealed by the Human, Mouse and Rat Genome Projects, and the finding that almost all known disease-associated genes have orthologs in mice and rats, perhaps the problem is our still-insufficient understanding of mechanisms and inadequate knowledge of species differences, resulting in poor choice of models, rather than in an inherent unsuitability of animal models to represent human disease.
Non-infectious uveitis is an inflammatory condition within the eye that has no known infection etiology. Uveitis is a heterogeneous disease: it can be a standalone condition affecting the eye only, or can be part of a more generalized systemic syndrome (see Table 1 for examples). Patients exhibit secondary responses to retinal antigens that are involved in vision and are unique to the eye, and have strong associations with HLA. The latter are associated with induction of immune responses because they present antigens to T cells. These findings have led to the notion that uveitis is autoimmune in nature, with particular HLA molecules presenting autologous retinal antigens that are normally sequestered within the eye, to the immune system. Additional support for this notion came from clinical findings that uveitis tends to respond clinically to T cell targeting agents (such as CsA, rapamycin, IL-2R, Campath — see Table 2) and that elevated inflammatory T cell responses of the Th1 and Th17 phenotypes often accompany the disease (Chi et al., 2008; Wang et al., 2012a). For ethical and logistic reasons, etiological agents and mechanistic associations are hard to study in humans. Nevertheless, animal models of uveitis induced by immunization with retinal antigens, or by transfer of retina-specific T cells (either Th1 or Th17) specific to these antigens, whose pathology is in many ways reminiscent of the human disease, would seem to support the notion that retina-specific T lymphocytes may be involved in driving disease pathology in humans.
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