EXPRESSION OF ICAM-R (ICAM-3), A NOVEL COUNTER-RECEPTOR FOR LFA-1, IN RHEUMATOID AND NONRHEUMATOID SYNOVIUM - COMPARISON WITH OTHER ADHESION MOLECULES
EXPRESSION OF ICAM-R (ICAM-3), A NOVEL COUNTER-RECEPTOR FOR LFA-1, IN RHEUMATOID AND NONRHEUMATOID SYNOVIUM - COMPARISON WITH OTHER ADHESION MOLECULES
复制标题
DOI：
10.1002/art.1780370612
复制
发表时间：
1994-06-01
影响因子：
--
通讯作者：
WILKINS, J
中科院分区：
文献类型：
--
作者：
ELGABALAWY, H;GALLATIN, M;WILKINS, J
Objective.研究白细胞整合素淋巴细胞功能相关抗原1（LFA-1）的新型配体细胞间粘附分子受体（ICAM-3）在正常和类风湿关节炎滑膜中的分布，并与ICAM-1、ICAM-2、血管细胞粘附分子1（VCAM-1）和内皮细胞粘附分子1（ELAM-1）的分布进行比较。我们用单克隆抗体对正常和类风湿性滑膜组织的冰冻切片进行免疫组化分析。ICAM-1在正常和类风湿性关节炎滑膜的血管内皮细胞和滑膜衬里细胞上均可检测到。不同比例的淋巴细胞浸润类风湿组织表达ICAM-1。ICAM-2染色在正常和炎症组织的血管内皮中均可见，后者显示阳性血管的比例显著较高。ELAM-1染色在正常滑膜中检测不到，但在有限数量的类风湿性滑膜血管的内皮上观察到，通常接近滑膜衬里细胞层。VCAM-1染色在正常和类风湿性滑膜衬里细胞中均较强，但血管染色较弱。相反，ICAM-R染色未检测到与任何滑膜血管相关，但广泛表达于淋巴细胞和巨噬细胞。衬里层细胞ICAM-R染色阴性。尽管ICAM-R是LFA-1的配体，并且与ICAM-1和ICAM-2具有相当大的序列同源性，但它似乎不被正常或发炎的滑膜血管的内皮表达。类风湿性滑膜淋巴细胞和巨噬细胞强烈表达ICAM-R，表明它可能在需要细胞-细胞接触的过程中发挥作用，如抗原呈递和同型聚集。
Objective. To study the distribution of intercellular adhesion molecule receptor (ICAM-R, or ICAM-3), a novel ligand for the leukointegrin lymphocyte function-associated antigen 1 (LFA-1), in normal and rheumatoid synovial membranes and to compare this with the distribution of ICAM-1, ICAM-2, vascular cell adhesion molecule 1 (VCAM-1), and endothelial leukocyte adhesion molecule 1 (ELAM-1).Methods. We performed immunohistochemical analyses of frozen sections of normal and rheumatoid synovial tissue using monoclonal antibodies to the molecules examined.Results. ICAM-1 staining was detectable on the vascular endothelium and the synovial lining cells of both normal and rheumatoid synovial membranes. A variable proportion of lymphocytes infiltrating rheumatoid tissues expressed ICAM-1. ICAM-2 staining was demonstrable in the vascular endothelium of both normal and inflamed tissues, the latter demonstrating a significantly higher proportion of positive vessels. ELAM-1 staining was not detectable in normal synovial membranes but was seen on the endothelium of a limited number of rheumatoid synovial vessels, usually close to the synovial lining cell layer. VCAM-1 staining was intense in both normal and rheumatoid synovial lining cells, but vascular staining was weak in both. In contrast, ICAM-R staining was not detected in association with any synovial blood vessels, but was widely expressed by lymphocytes and macrophages. Cells of the lining layer did not stain for ICAM-R.Conclusion. Although ICAM-R is a ligand for LFA-1 and shares considerable sequence homology with ICAM-1 and ICAM-2, it does not appear to be expressed by the endothelium of normal or inflamed synovial vessels. Intense expression of ICAM-R by rheumatoid synovial lymphocytes and macrophages suggests that it may play a role in processes requiring cell-cell contact, such as antigen presentation and homotypic aggregation.