ABSTRACT
The immunopathologic response following the injection of various antigens into the rat cornea was evaluated. This reaction, known as Wessely's phenomenon, was believed to be primarily triggered by antibodies and complement activation. The keratitis model was originally described in rabbits, using heterologous serum or purified proteins. In rats only, heterologous serum induced corneal inflammation with the characteristics of Wessely's phenomenon, (ie, a quiescent period of several days between antigen injection and onset of clinical signs and corneal opacification). Using rats allowed us to characterize the cellular infiltrate with immunohistochemical methods. Marked infiltration of the cornea by macrophages was observed, as was infiltration by polymorphonuclear cells, although to a lesser extent. Furthermore, T lymphocytes of the helper phenotype were demonstrated. Antibodies to complement activation product C3c showed faint staining, whereas B lymphocytes and plasma cells were absent. In addition, inflammatory cells and ocular tissues, particularly the limbal and peripheral corneal epithelium, were found to express major histocompatibility complex class II antigens during the inflammatory response. After the inflammation had subsided, macrophages and T lymphocytes remained in the corneal stroma (at least until day 30). These findings suggest that antigen-induced keratitis in rats might be mediated, at least partially, by T helper lymphocytes.
Subject(s)
Corneal Stroma/immunology , Keratitis/immunology , Animals , Antibodies, Monoclonal , B-Lymphocytes/immunology , Blood , Complement C3c/immunology , Histocompatibility Antigens Class II/immunology , Immunoenzyme Techniques , Immunoglobulin G/administration & dosage , Immunophenotyping , Injections , Keratitis/pathology , Lipopolysaccharides/administration & dosage , Lymph Nodes/immunology , Macrophages/immunology , Male , Rats , Rats, Inbred BN , T-Lymphocytes/immunology , T-Lymphocytes, Helper-Inducer/immunologyABSTRACT
The pathogenesis of peripheral corneal lesions of immune aetiology, like Mooren's ulcer and catarrhal infiltrates, has been related to the formation or deposition of immune compkexes. The present investigation was undertaken to study the mechanisms involved in the elimination of immune precipitates from the cornea. Immune precipitates were induced by injecting human serum albumin (HSA) and rabbit anti-HSA serum into opposite sites of the rat corneal stroma. This resulted in a line-shaped opacity in the stroma, which remained visible by slit-lamp for 7 days, and disappeared without clinical signs of keratitis and uveitis. At the ultrastructural level, the immune precipitates were clearly visible. Keratocytes in the vicinity of the immune precipitates appeared activated, as suggested by their less flattened appearance and well-developed rough endoplasmic reticulum. The arrangement of the collagen fibrils was not affected. Cells with a macrophage-like morphology were also present and contained electron-dense material, closely resembling the precipitate, suggesting phagocytosis. Separate corneas were injected with latex beads, which is known to induce migration of Langerhans cells into the cornea. Immunohistochemical analysis revealed that both latex beads and immune precipitates induced migration of macrophages (ED1+) into the rat corneal stroma. However, differences were observed with regard to the expression of MHC class II antigens by these ED1+ cells and the presence of complement deposits in the corneal stroma. ED1+ cells in corneas injected with latex beads were all MHC class II positive (OX4+), whereas most of the ED1+ cells at the site of the immune precipitates were negative (OX4-).(ABSTRACT TRUNCATED AT 250 WORDS)
