细胞粘附分子在炎症角膜中的表达

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（ｉｎｔｅｒｃｅｌｕｌａｒａｄｈｅｓｉｏｎｍｏｌｅｃｕｌｅ１，ＩＣＡＭ１）、人类白细胞抗原ＤＲ（ｈｕｍａｎｌｅｕｋｏｃｙｔｅａｎｔｉｇｅｎＤＲ，ＨＬＡＤＲ）、ＣＤ１１ａ、ＣＤ１１ｂ、ＣＤ１８、ＣＤ２和ＣＤ２０的表达及变化。结果：正常角膜中，ＩＣＡＭ１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ＩＣＡＭ１表达增强，尤其在炎症细胞浸润处最为显著；原不表达ＩＣＡＭ１的上皮细胞亦出现异常表达；ＩＣＡＭ１和ＨＬＡＤＲ常共同表达于同一部位，炎症明显组角膜ＩＣＡＭ１和ＨＬＡＤＲ的表达水平明显高于炎症轻微组；炎症浸润细胞中表达ＬＦＡ１（ＣＤ１１ａ／ＣＤ１８）的细胞较表达Ｍａｃ１（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

Expression of cell adhesion molecules in human inflamed corneas

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.