Circulating anti-galectin-1 antibodies are associated with the severity of ocular disease in autoimmune and infectious uveitis.

PURPOSE: Galectin (Gal)-1, an endogenous lectin found at sites of immune privilege, plays a critical role in the regulation of the immune response. Therapeutic administration of Gal-1 or its genetic delivery suppresses chronic inflammation in experimental models of autoimmunity. The purpose of this work was to investigate the occurrence of circulating anti-Gal-1 antibodies in patients with autoimmune and infectious uveitis as potential determinant factors of disease progression. METHODS: IgG, IgE, and IgA anti-Gal-1 antibodies were assessed by ELISA and Western blot in sera from patients with autoimmune (n = 47) and infectious (n = 15) uveitis compared with healthy control subjects (n = 30). The frequency of anti-Gal-1 antibodies was examined in patients experiencing poor clinical outcome (n = 21) or good evolution (n = 9). Anti-Gal-1 antibodies were eluted by incubating patient sera with nitrocellulose filters adsorbed with rGal-1. The ability of these antibodies to recognize retinal tissue was assessed by ELISA, Western blot, and immunohistochemistry. RESULTS: IgE, IgG, and IgA anti-Gal-1 antibodies were increased in sera from patients with autoimmune uveitis (P < 0.001 vs. controls) and toxoplasmic retinochoroiditis (P < 0.001). The level of anti-Gal-1 IgE and IgG antibodies was associated with progressive disease and poor outcome in autoimmune and infectious uveitis. Furthermore, these antibodies strongly immunoreacted with retinal lysates and recognized retinal structures mainly photoreceptors in retinal sections. CONCLUSIONS: Anti-retinal Gal-1 antibodies are present in sera from patients with uveitis and can be associated with the progression of ocular disease, suggesting their potential use in follow-up observations of these patients.

The importance of specific IgG and IgE autoantibodies to retinal S antigen, total serum IgE, and sCD23 levels in autoimmune and infectious uveitis.

Autoimmunity plays an important role in the development of uveitis. The uveitis are linked to Th1 or Th2 lymphocyte activation. We studied 41 patients with uveitis, divided into autoimmune uveitis (n = 32) and infectious uveitis (n = 9), 30 normal controls, and 20 asthmatic atopic without ocular diseases. The infectious uveitis patients were separated into bacterial (n = 6) and toxoplasmic (n = 3) retinochoroiditis. We measured IgE and sCD23 serum levels and specific IgG and IgE to retinal S antigen by ELISA tests. The IgE levels were 500 +/- 325 kU/L in autoimmune uveitis, 57 +/- 35 kU/L in bacterial uveitis, 280 +/- 38 kU/L in toxoplasmic retinochoroiditis, 75 +/- 32 kU/L in the controls, and 557 +/- 243 kU/L in atopics (P < 0.0005). The sCD23 levels were 10.4 +/- 5.4 ng/ml in autoimmune uveitis, 3.7 +/- 1.17 ng/ml in bacterial uveitis, 6.76 +/- 1.36 ng/ml in toxoplasmic retinochoroiditis, 3.4 +/- 1 ng/ml in controls, and 8.35 +/- 2.2 ng/ml in atopic patients (P < 0.005). The specific IgG to retinal S antigen was positive in 27 of 32 cases, and the specific IgE to retinal S antigen was positive in 22 of 32 autoimmune uveitis. The bacterial uveitis patients as well as the controls were negative for both autoantibodies to retinal S antigen. The toxoplasmic retinochoroiditis patients presented specific IgG and IgE to retinal S antigen in two of three cases, respectively, one of them with overlap of both antibodies. These results suggest the importance of specific IgG and IgE to retinal S antigen in autoimmune uveitis, which, along with higher IgE and sCD23 levels, reveal Th2 activation.