摘要
目的:研究细胞粘附分子(celularadhesionmolecules,CAMs)在炎症角膜中的表达,探讨其在角膜炎症发生机制中的作用。方法:采用冰冻切片免疫组织化学染色方法检测了18只炎症角膜、3只正常角膜和2只圆锥角膜组织中细胞间粘附分子1(intercelularadhesionmolecule1,ICAM1)、人类白细胞抗原DR(humanleukocyteantigenDR,HLADR)、CD11a、CD11b、CD18、CD2和CD20的表达及变化。结果:正常角膜中,ICAM1主要表达于角膜缘血管内皮细胞,基质细胞、角膜内皮细胞中仅有微弱表达或不表达。炎症角膜中,基质细胞、内皮细胞和血管内皮细胞的ICAM1表达增强,尤其在炎症细胞浸润处最为显著;原不表达ICAM1的上皮细胞亦出现异常表达;ICAM1和HLADR常共同表达于同一部位,炎症明显组角膜ICAM1和HLADR的表达水平明显高于炎症轻微组;炎症浸润细胞中表达LFA1(CD11a/CD18)的细胞较表达Mac1(CD11b/CD18)的细胞多;浸润淋巴细胞以T(CD2)淋巴细胞为主;属非炎症性病变的圆锥角膜中I?
Objective: To detect the expression level of cell adhesion molecules (CAMs) in inflammatory corneas for investigation of the role they play in the pathogenic mechanisms of corneal inflammation. Methods: The expression and changes of intercellular adhesion molecule 1 (ICAM 1), human leukocyte antigen DR (HLA DR), LFA 1, Mac 1, CD2 and CD20 were examined in 18 inflammatory corneas, 3 normal corneas and 2 keratoconus frozen section using immunohistochemical staining method. Results: In normal corneas, ICAM 1 was mainly found on limbal vascular endothelial cells, and weakly or not expressed on stromal keratocytes and corneal endothelium. Inflamed corneas showed increased ICAM 1 expression on stromal keratocyte, corneal, and vascular endothelium, particularly in the sites of leukocytes infiltration. Epithelial cells which didn't express ICAM 1 constitutively began to express ICAM 1. ICAM 1 and HLA DR usually co expressed in similar regions. The level of ICAM 1 and HLA DR expression in obviously inflamed cornea groups was significantly higher than that in slightly inflamed cornea groups. The number of infiltrative leukocytes that were positive for LFA 1 was more than that of cells that were positive for Mac 1. The lymphocytes of inflamed cornea consisted predominantly of T cells. Non inflamed keratoconus showed similar expression pattern to normal corneas. Conclusion: The increased expression of CAMs in inflamed corneas has parallel migrating with the extent of inflammation. CAMs may play a critical role in regulating leukocytes migrating and accumulating at sites of inflammation, thereby generating inflammatory response and damage of tissue.
出处
《北京医科大学学报》
CSCD
1999年第1期79-82,共4页
Journal of Peking University(Health Sciences)
关键词
细胞粘着分子
代谢
角膜炎症
病理生理学
Cell adhesion molecules/metab Cornea/metab Keratitis/physiopathol