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.