IMMUNOPATHOLOGY IN EYES WITH EXPERIMENTAL AND CLINICAL OCULAR DISEASES

的身份和地形定位 免疫活性细胞和细胞标志物的改变 各种实验性葡萄膜炎动物的眼驻留细胞 通过免疫组织化学，原位杂交， 聚合酶链反应（PCR）。此前，我们有 表明T淋巴细胞是主要的浸润性细胞， 实验性自身免疫性葡萄膜视网膜炎和实验性 黑色素诱导的葡萄膜炎，包括巨噬细胞和多形核细胞 中性粒细胞是主要的浸润细胞， 内毒素诱导的葡萄膜炎，而所有类型的白细胞都存在 小鼠实验性睑缘炎。细胞因子和炎症 介质在免疫发病机制中起重要作用， 眼部炎症主要组织相容性类表达 (MHC)II抗原、粘附分子和凋亡标志物是 在炎症过程中在眼驻留细胞上观察到。 在1998财政年度，我们确定了Th 1和Th 2的动力学 两种动物眼内细胞因子Fas、FasL、bcl-2和Bax的表达 模型和葡萄膜炎的人类标本。使用显微切割 和PCR，我们已经确定了免疫球蛋白的重排， 原发性眼内肿瘤重链基因和bcl-2易位 淋巴瘤细胞这些淋巴瘤细胞也产生IL-10 mRNA IL-10的检测有助于诊断。我们有 证明了视网膜血管瘤中的泡沫状“基质”细胞， von Hippel-Lindau（VHL）病具有VHL基因缺失， 肿瘤抑制基因因此，它降低了正常的VHL 干扰延伸蛋白并诱导血管生成的蛋白质翻译 内皮生长因子促进新生血管形成。的 显微切割和分子技术的结合 来研究选择性的微小细胞群及其遗传学。 阐明免疫病理学作用的关系 在浸润细胞和眼驻留细胞之间的相互作用将有助于 更好地了解和管理各种眼科疾病， 患者

The identity and topographic localization of immunocompetent cells and the alteration of cellular markers on ocular resident cells in animals with various experimental uveitis were analyzed by immunohistochemistry, in situ hybridization, and polymerase chain reaction (PCR). Previously, we have demonstrated that T lymphocytes are the predominant infiltrating cells in experimental autoimmune uveoretinitis and experimental melanin-induced uveitis, both macrophages and polymorphonuclear neutrophils are the predominant infiltrating cells in endotoxin-induced uveitis, while all types of leukocytes are present in murine experimental blepharitis. Cytokines and inflammatory mediators play an important role in the immunopathogenesis of ocular inflammation. Expressions of major histocompatibility class (MHC) II antigens, adhesion molecules and apoptotic markers are observed on ocular resident cells during the inflammatory process. In FY1998 we have identified the kinetics of Th1 and Th2 cytokines, Fas, FasL, bcl-2 and Bax in the eyes of both animal models and human specimens with uveitis. Using microdissection and PCR, we have identified rearrangement of the immunoglobulin heavy chain gene and bcl-2 translocation in primary intraocular lymphoma cells. These lymphoma cells also produce IL-10 mRNA and IL-10 in the vitreous which can aid diagnosis. We have demonstrated the foamy "stromal" cells in the retinal angioma of von Hippel-Lindau (VHL) disease have loss of the VHL gene, a tumor suppressor gene. In consequence it decreases normal VHL protein translation that interferes with elongin and induce vascular endothelium growth factor to promote neovascularization. The combination of microdissection and molecular techniques helps us to study the selective minute population of cells and their genetics. Elucidating the immunopathological role of the relationship between the infiltrating cells and ocular resident cells will aid in better understanding and management of various ocular diseases in patients.