Autoimmunity and the outer retina

Structurally and therefore antigenically the retina is a complex tissue. Since it develops as an extension from the neural tube it shares with the brain several cell membranes and cytoplasm associated antigens including those present in neurofilaments of the various neurones and the glial filaments of the astrocytes. The advent of monoclonal antibodies has helped to dissect, in detail, the antigenic makeup of the retina. Nervous system antigens (NS-3, 4 and 7) are generously represented in the retina. At least in the chick eye there seems to be a concentration gradient of retinal antigens along a dorsoventral axis which is believed to provide means by which neurones of developing retinal signal and receive the positional information necessary for the formation of specific synapses. It now seems certain that organ-specific antigens are presented not only in the photoreceptors and the retinal pigment epithelium but also in the retinal ganglion cells and the astrocytes. Photoreceptor outer-segment contains soluble antigens which when injected in rats, rabbits, guinea-pigs or monkeys produce varying degrees of intraocular inflammation leading to uveitis, retinal detachment, photoreceptor degeneration and occasionally retinal vasculitis. Both cell-mediated and humoral immunity to photoreceptor antigen has been demonstrated in various types of uveitis (including toxoplasmosis and sarcoidosis), pars planitis, vitriitis, Behçets disease, sympathetic ophthalmitis, Vogt-Koyanagi-Harada syndrome, birdshot retinopathy, retinitis pigmentosa and retinal vasculitis. Retinal autoimmunity is also found in retinal detachment and diabetic retinopathy, particularly after Argon laser photocoagulation. Antibodies to retinal antigens are also found in patients with systemic lupus erythematosus and other systemic immune disorders without ocular involvement. The precise pathogenetic role of retinal autoimmunity in eye disease is therefore uncertain. It may simply represent an epiphenomenon which develops afer retinal damage due to physical, micro-organismal or immunological insult. Alternatively it is possible that although autoimmunity does not initiate ocular inflammation it perpetuates and maintains the inflammatory state and produces further damage to ocular tissues.