Abu el-Asrar A M, Geboes K, Tabbara K F, van den Oord J J, Missotten L
Department of Ophthalmology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
Bull Soc Belge Ophtalmol. 1996;261:15-24.
We have analyzed the in situ distribution of immune cells in the conjunctival biopsy specimens obtained from patients with active vernal keratoconjunctivitis (VKC). We used immunohistochemical techniques and a panel of monoclonal and polyclonal antibodies. Our data point to a complex immunopathogenesis of the disease. Distinct components involved in IgE-mediated immune mechanisms, as well as humoral and cell mediated immune mechanisms were detected in the conjunctival tissues. In addition, we investigated the presence and distribution of adhesion molecules. In the normal conjunctiva, intercellular adhesion molecule-1 (ICAM-1) was expressed only on the vascular endothelium, lymphocyte function associated antigen-1 (LFA-1) and intercellular adhesion molecule-3 (ICAM-3) on epithelial and stromal mononuclear cells, and very late activation antigen-4 (VLA-4) on a few stromal mononuclear cells. Endothelial leukocyte adhesion molecule-1 (ELAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression was not detected. In VKC a marked increase of all these antigens was observed. Strong ICAM-1 expression was induced on the basal epithelial cells, and vascular endothelium. Furthermore, about 30% of the stromal mononuclear cells expressed ICAM-1. LFA-1 and ICAM-3 were expressed on the majority of infiltrating mononuclear cells. VLA-4 expression was noted on about 25% of the stromal mononuclear cells. ELAM-1 and VCAM-1 were induced on the vascular endothelial cells. Our results suggests that increased expression of adhesion molecules in VKC promotes the recruitment of inflammatory cells through blood vessels and the cell interaction between lymphocytes and antigen presenting cells, among lymphocytes, as well as between lymphocytes and epithelial cells.
我们分析了从活动性春季角结膜炎（VKC）患者获取的结膜活检标本中免疫细胞的原位分布。我们使用了免疫组织化学技术以及一组单克隆和多克隆抗体。我们的数据表明该疾病存在复杂的免疫发病机制。在结膜组织中检测到了参与IgE介导的免疫机制以及体液和细胞介导的免疫机制的不同成分。此外，我们研究了黏附分子的存在和分布。在正常结膜中，细胞间黏附分子-1（ICAM-1）仅在血管内皮细胞上表达，淋巴细胞功能相关抗原-1（LFA-1）和细胞间黏附分子-3（ICAM-3）在上皮和基质单核细胞上表达，而极晚期活化抗原-4（VLA-4）在少数基质单核细胞上表达。未检测到内皮白细胞黏附分子-1（ELAM-1）和血管细胞黏附分子-1（VCAM-1）的表达。在VKC中，观察到所有这些抗原均显著增加。在基底上皮细胞和血管内皮细胞上诱导了强烈的ICAM-1表达。此外，约30%的基质单核细胞表达ICAM-1。LFA-1和ICAM-3在大多数浸润的单核细胞上表达。约25%的基质单核细胞上有VLA-4表达。在血管内皮细胞上诱导了ELAM-1和VCAM-1的表达。我们的结果表明，VKC中黏附分子表达的增加促进了炎症细胞通过血管的募集以及淋巴细胞与抗原呈递细胞之间、淋巴细胞之间以及淋巴细胞与上皮细胞之间的细胞相互作用。
