Verhagen C, Den Heijer R, Klooster J, Breebaart A C, Kijlstra A
Department of Ophthalmology, University of Amsterdam, The Netherlands.
Exp Eye Res. 1991 Oct;53(4):471-8. doi: 10.1016/0014-4835(91)90164-a.
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)
免疫病因导致的周边角膜病变,如蚕蚀性角膜溃疡和卡他性浸润,其发病机制与免疫复合物的形成或沉积有关。本研究旨在探讨角膜清除免疫沉淀物所涉及的机制。通过将人血清白蛋白(HSA)和兔抗HSA血清注射到大鼠角膜基质的相对部位来诱导免疫沉淀物形成。这导致基质中出现线状混浊,裂隙灯检查可见该混浊持续7天,之后消失,且无角膜炎和葡萄膜炎的临床症状。在超微结构水平上,免疫沉淀物清晰可见。免疫沉淀物附近的角膜细胞似乎被激活,表现为形态不再扁平且粗面内质网发达。胶原纤维的排列未受影响。还存在具有巨噬细胞样形态的细胞,其含有电子致密物质,与沉淀物极为相似,提示存在吞噬作用。向单独的角膜注射乳胶珠,已知乳胶珠可诱导朗格汉斯细胞迁移至角膜。免疫组织化学分析显示,乳胶珠和免疫沉淀物均可诱导巨噬细胞(ED1 +)迁移至大鼠角膜基质。然而,在这些ED1 +细胞的MHC II类抗原表达以及角膜基质中补体沉积物的存在方面观察到了差异。注射乳胶珠的角膜中的ED1 +细胞均为MHC II类阳性(OX4 +),而免疫沉淀物部位的大多数ED1 +细胞为阴性(OX4 -)。(摘要截短于250字)