Beta 1 (CD29) integrin expression in rheumatoid synovial membranes: an immunohistologic study of distribution patterns.
Beta 1 (CD29) integrin expression in rheumatoid synovial membranes: an immunohistologic study of distribution patterns.
复制标题
类风湿滑膜中的 Beta 1 (CD29) 整合素表达：分布模式的免疫组织学研究。
作者：
H. El Gabalawy;J. Wilkins
细胞附着和迁移到组织中是炎症过程的关键方面。我们的研究是为了检测黏附分子家族之一的β1整合素(VLA抗原)在炎症类风湿滑膜组织中的分布。应用免疫组织化学和单克隆抗体对10例类风湿滑膜中淋巴细胞亚群和β1整合素(β1、VLA-1、2、3、4、5)的分布进行了研究。大多数淋巴细胞表达β1、VLA-3、VLA-4和VLA-5。与血管外间隙相比，附着在血管内皮细胞上的单个核细胞通常表达较低水平的β1，这表明淋巴细胞在渗入组织后可能会增强这种分子的表达。滑膜衬里层细胞表达β1、VLA-1、VLA-3和VLA-5。滑膜血管内皮细胞表达β1、VLA-1、VLA-3和VLA-5，VLA-2染色较少。滑膜下淋巴细胞集合体内及周围的小静脉和毛细血管的血管染色最深。我们的结论是，β1整合素在类风湿滑膜中由多种细胞表达。β1整合素的表达可能受到炎症微环境的调节，从而有助于形成更具粘附性的环境，使炎症细胞更容易被招募和保留。
Cellular attachment to, and migration into, tissues are critical aspects of the inflammatory process. Our studies were undertaken to examine the distribution of one of the families of adhesion molecules, the beta 1 integrins (VLA antigens), in inflamed rheumatoid synovial tissues. The distribution of lymphocyte subsets and the beta 1 integrins (beta 1, VLA-1, 2, 3, 4, 5) were studied in 10 rheumatoid synovial membranes using immunohistochemistry and monoclonal antibodies. The majority of lymphocytes stained positively for beta 1, VLA-3, VLA-4 and VLA-5. Intravascular mononuclear cells adherent to the endothelium appeared to generally express low levels of beta 1 when compared to those in the extravascular space, suggesting that lymphocytes may augment their expression of this molecule subsequent to their extravasation into the tissue. Cells in the synovial lining layer expressed beta 1, VLA-1, VLA-3 and and VLA-5. The endothelium of the synovial vasculature stained intensely for beta 1, VLA-1, VLA-3 and VLA-5 with more limited staining for VLA-2. The venules and capillaries in and around the subsynovial lymphocytic aggregates demonstrated the most intense vascular staining. We conclude that the beta 1 integrins are expressed by a variety of cells in the rheumatoid synovial membrane. The expression of beta 1 integrins may be subject to regulation by the inflammatory microenvironment thus contributing to a more adhesive environment into which inflammatory cells are more readily recruited and retained.