Elimination of immune precipitates from the rat corneal stroma: a histological study

Abstract

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 complexes. 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 −). Deposits of the complement activation product C3c were present in the immune complex model, but absent in the latex beads-induced reaction. These data demonstrate that immune precipitates induce migration of macrophages into the cornea, and that expression of MHC class II antigens by these cells is non-uniform. This variability may reflect the presence of subtypes of macrophages or different stages of maturation, or may be due to local stimuli like phagocytosis or complement activation.