Autoimmune and immunemediated eye diseases in humans

Although strong associations have been noted between many uveitic diseases and HLA type, indicating an immunogenetic component to disease etiology, the extent to which autoimmunity in the strict sense plays a role in human disease is still controversial. The reason for this is that in most cases the eliciting antigens have not yet been positively identified. One exception is phacoanaphylaxis, caused by an autoimmune response to lens proteins, usually following trauma and disruption of the lens capsule. Lens-specific antibodies and complement activation appear to be intimately involved in the disorder, but it is still unknown whether a significant cell-mediated component exists. In animal models of lens-induced uveitis (LIU), a primarily humoral mechanism of disease has been demonstrated.

In posterior uveitic disease, sympathetic ophthalmia (SO) has for a long time been considered the prototypic ocular autoimmune disease. As in phacoanaphylaxis, pathogenesis can be linked to a discrete inducing event, i.e. a penetrating trauma to one eye. Characteristic of SO is the subsequent development, weeks to months later, of an acute inflammation in the contralateral (sympathizing) eye, which has not been injured. This has been attributed to the development of an autoimmune response to the ocular antigens released into the bloodstream from the injured (exciting) eye. It is unclcar why SO develops in only a small proportion of the cases ot ocular trauma, and what the predisposing factors are. Genetic susceptibility and a concomitant adjuvant effect due to infection have been proposed as possible facilitating mechanisms. Additional posterior and intermediate uveitic diseases for which an autoimmune component(s) has been postulated include birdshot retinochoroidopathy, and systemic diseases with ocular involvement, such as Behcet's disease and Vogt-Koyanagi-Harada syndrome. Many patients suffering from these diseases display strong immunologic responses to retinal proteins. Of particular note, a number of studies that demonstrated specific antibody and lymphocyte responses to the retinal soluble antigen (S-Ag) in birdshot retinochoroidopathy patients and in other uveitis patients. Although it is difficult to determine to what extent these responses might play a role in the etiology and/or pathogenesis of their disease, the S-Ag is one of several retinal proteins which cause experimental autoimmune uveoretinitis in laboratory animals (see below). Antigens that might be involved in anterior uveitic disease affecting the iris and ciliary body arc also yet to be identified, but at least one type of anterior uveitis (the Reiter syndrome! has been linked to the presence of anti-Klehsielhi responses in the affected patients (see below).

Animal models of uveitis, elicited by immunization with eye-derived proteins, have been developed and serve as research tools that have yielded invaluable insights into the mechanisms and therapy of these sight-threatening ocular inflammatory diseases (Table 1).

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