Complement activation in the aqueous humor of pseudophakic bullous keratopathy patients.

BACKGROUND/AIMS: According to some studies, inflammation is a potential etiological factor in pseudophakic bullous keratopathy (PBK). Our aim was to obtain information on the activation of the complement system in the aqueous humor in this disorder. METHODS: Aqueous humor samples were collected during keratoplasty of 12 PBK patients, as well as during phacoemulsification surgery of 18 control patients. The concentrations of the protein-protein complexes generated during complement activation (C1rC1sC1inh and C3bBbP) through the classical and alternative pathways, respectively, as well as of the C3 cleavage product C3a, were measured with ELISA methods. The correlation among the complement factors and between the duration of the edema, the stage of the disease, and the level of the complement activation products was examined. RESULTS: The concentration of C1rC1sC1inh, C3bBbP complex and C3a was significantly higher in the PBK group (p < 0.001) compared to the control group. In PBK patients, a correlation was found between the levels of the C1rC1sC1inh complex and C3a only. CONCLUSION: Our new findings indicate that in PBK the complement system is activated - via the classical pathway - in the aqueous humor. The activated complement may play a role in increased endothelial cell loss.

Expression of HLA-G in human cornea, an immune-privileged tissue.

Human leukocyte antigen (HLA)-G retains the capacity to modulate immune responses, favoring the establishment of tolerance in solid-tissue allotransplants. To better understand the mechanisms that promote corneal allograft survival, we investigated whether HLA-G was an immunoregulatory factor involved in corneal immunology. We therefore sought HLA-G expression in corneal tissues. Corneal transplantation consists in replacing the center of a diseased cornea with normal corneal tissue. Two corneal parts are not used in such surgery: diseased central corneal tissue and peripheral normal cornea. For this study, we used healthy corneas obtained from deceased donors and diseased corneas obtained from patients with pseudophakic bullous keratopathy or keratoconus who had undergone corneal transplantation. Immunohistochemical analysis carried out on the cryopreserved corneas showed a positive immunohistochemical staining with anti-HLA-G, anti-HLA-A, -B, and -C, and anti-HLA class I monoclonal antibodies. Staining was obtained for keratocytes, epithelial cells, and endothelial cells from both healthy and pathologic human corneas, revealing the presence of HLA class I proteins, including HLA-G. HLA-G transcripts were detected in normal cornea by reverse transcriptase-polymerase chain reaction with a classical pattern of alternative splicing. The detection of HLA-G protein in adult corneas leads to the conclusion that this protein may contribute to the maintenance of the privileged immune status of cornea.