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Autoimmune reactivity and autoimmune disease in the eye is a rapidly expanding area of research and therapy. We present evidence implicating three distinct classes of infectious agents in the development of an autoimmune process within the retina. We highlight two human diseases triggered by Onchocerca volvulus or Toxoplasma gondii and an experimental model of retinal degenerative disease, referred to as experimental coronavirus retinopathy (ECOR). Analysis of these systems revealed distinct pathogenic mechanisms involved in the induction of autoimmunity triggered by each organism. In T. gondii infections, the chronic reactivation is probably responsible for the presentation of sequestered retinal epitopes of the immune system. In O. volvulus infections, molecular mimicry between the organism and the human RPE protein may contribute to retinal pathology. In ECOR, differences in time of induction, duration, and intensity of innate immune reactivity may contribute to autoimmune reactivity in BALB/c mice.

SUMMARY Immune response to retinal autoantigens plays a central role in the pathogenesis of uveitis. A synthetic peptide (B27PD) from a common sequence of various HLA-B molecules associated with uveitis, such as HLA-B27 and 51, which shares amino acid homologies with a retinal-S antigen (S-Ag)-derived peptide (PDSAg), was shown to be immunogenic in human and experimental uveitis in the rat. In this study we investigated T cell responses to B27PD and PDSAg in patients with Behçet’s disease and posterior uveitis (BD-posterior uveitis; n = 33) in comparison with non-Behçet anterior uveitis (AU, n = 14), Behçet’s patients without uveitis (BD, n = 15) and healthy controls (HC, n = 32) in a 6-day proliferation assay. Patients with BD and posterior uveitis had significantly higher responses (stimulation index (SI) 2·8 ± 1·3) than those with AU (SI 1·5 ± 0·4), BD without uveitis (SI 1·1 ± 0·4) and HC (SI 1·1 ± 0·6) for B27PD (P