Anti-retinal autoantibodies in experimental ocular and systemic toxoplasmosis.

Background: Patients with ocular toxoplasmosis (OT) develop autoreactivity to several retinal antigens, including retinal S-antigen. By establishing an experimental rabbit model of systemic and of primary and secondary ocular toxoplasmosis, we wished to investigate the onset and development of humoral response to retinal S-antigen.

Methods: Of twelve infection-naïve rabbits, six were left untreated, and the other six were infected subcutaneously with 5,000 tachyzoites of the highly virulent, non-cyst-forming BK-strain of Toxoplasma gondii. Three months later, the left eye of each animal was infected transvitreally with 5,000 tachyzoites of the same strain. The right eye of each rabbit served as an uninfected control. Blood and aqueous humor were collected prior to infection, and up to 90 days thereafter. Using the ELISA technique, all samples were analyzed in parallel for total IgG, and antibodies against toxoplasmic, bovine retinal S-antigen and peptide 35 from human S-antigen.

Results: In infection-naïve rabbits Toxoplasma-specific antibodies were detected 10 to 15 days after systemic and ocular infection. Serum antibodies against retinal S-antigen and peptide 35 were not detected in response to systemic Toxoplasma infection. After ocular challenge, aqueous-humour levels of antibodies against retinal S-antigen and peptide 35 in the infected eye began to rise 10 to 15 days later in infection-naïve, but not in infection-immunized animals. During the early post-infection period, the concentrations of anti-retinal antibodies in the infected eye correlated with the severity of inflammatory tissue destruction, but returned to baseline later even though the inflammatory response persisted. In the uninfected partner eye, concentrations of anti-retinal and toxoplasmic antibodies did not correlate with each other.

Conclusion: Our data afford no evidence of similarities between toxoplasmic and retinal antigens, nor of infection-induced humoral autoimmunity. They indicate rather that retinal autoantigens are liberated in the context of inflammatory tissue destruction due to ocular toxoplasmosis.