Regezi J A, Dekker N P, MacPhail L A, Lozada-Nur F, McCalmont T H
Department of Stomatology, School of Dentistry, University of California, San Francisco, USA.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996 Jun;81(6):682-90. doi: 10.1016/s1079-2104(96)80074-6.
Because recruitment and retention of lymphoid cells appear to be critical components of the pathogenesis of lichen planus, we have compared the expression and distribution of a panel of vascular adhesion molecules (ELAM-1, P-selectin, ICAM-1, VCAM-1, PECAM-1, CD34) and leukocyte adhesion molecule ligands (LFA-1, Mac-1, VLA4, L-selectin) in biopsies of this disease.
STUDY-DESIGN: Frozen sections of 12 clinically and histologically confirmed cases of lichen planus and 9 normal control tissues were evaluated immunohistochemically with a standard 1-day avidin-biotin peroxidase technique. Staining intensity of vascular endothelium was evaluated semiquantitatively. Three microvascular zones or compartments were defined and evaluated separately.
Generally, different staining patterns were observed in association with the various endothelium-associated adhesion molecules. In normal controls, PECAM was intensely expressed and VCAM-1 was weakly expressed. Intermediate staining was associated with ELAM-1, P-selectin, ICAM-1, and CD34. Staining within the three microvascular compartments frequently showed variations in intensity. In lichen planus, increased staining for ELAM-1, P-selectin, ICAM-1, and VCAM-1 was evident in one or more of the microvascular compartments. In the subepithelial vascular compartment where the infiltrate was the most dense, VCAM-1 appeared to show the greatest positive change. Almost all cells in the lichen planus infiltrates stained positive for ICAM-1, L-selectin, LFA-1, and VLA4, and large numbers of cells also exhibited VCAM-1, PECAM-1, and Mac-1 immunoreactivity.
It appears that upregulation of ELAM-1, ICAM-1, and VCAM-1 (especially by endothelial cells in the subepithelial vascular plexus) could play a role in the pathogenesis of lichen planus. The expression of leukocyte receptors L-selectin, LFA-1, and VLA4 by most of the cells in the lichen planus infiltrate suggest that these molecules may be responsible for recruitment as well as retention in the active lichen planus lesion.
由于淋巴细胞的募集和留存似乎是扁平苔藓发病机制的关键组成部分，我们比较了一组血管黏附分子（ELAM-1、P-选择素、ICAM-1、VCAM-1、PECAM-1、CD34）和白细胞黏附分子配体（LFA-1、Mac-1、VLA4、L-选择素）在该病活检组织中的表达及分布情况。
采用标准的一日抗生物素蛋白-生物素过氧化物酶技术，对12例临床和组织学确诊的扁平苔藓病例及9例正常对照组织的冰冻切片进行免疫组织化学评估。对血管内皮的染色强度进行半定量评估。定义并分别评估三个微血管区域或腔隙。
一般来说，与各种内皮相关黏附分子相关的染色模式不同。在正常对照中，PECAM表达强烈，VCAM-1表达较弱。中等强度染色与ELAM-1、P-选择素、ICAM-1和CD34相关。三个微血管腔隙内的染色强度常常显示出差异。在扁平苔藓中，ELAM-1、P-选择素、ICAM-1和VCAM-1在一个或多个微血管腔隙中的染色增加明显。在浸润最密集的上皮下血管腔隙中，VCAM-1似乎显示出最大的阳性变化。扁平苔藓浸润中的几乎所有细胞对ICAM-1、L-选择素、LFA-1和VLA4染色呈阳性，并且大量细胞也表现出VCAM-1、PECAM-1和Mac-1免疫反应性。
ELAM-1、ICAM-1和VCAM-1（特别是上皮下血管丛中的内皮细胞）的上调似乎可能在扁平苔藓的发病机制中起作用。扁平苔藓浸润中的大多数细胞表达白细胞受体L-选择素、LFA-1和VLA4，这表明这些分子可能负责活跃扁平苔藓病变中的细胞募集和留存。
