IMMUNOPATHOLOGY IN EYES WITH EXPERIMENTAL AND CLINICAL OCULAR DISEASES

免疫活性细胞的特性和地形图定位 动物眼内停留细胞表面细胞标志物的变化 用免疫组织化学方法对各种实验性葡萄膜炎进行分析 和原位杂交。之前，我们已经演示了T 淋巴细胞，特别是cd4细胞占主导地位。 实验性自身免疫性葡萄膜视网膜炎(EAU)和 实验性黑色素蛋白诱导性葡萄膜炎(EMIU)，但两种巨噬细胞 中性粒细胞是主要的浸润性细胞。 在内毒素诱导的葡萄膜炎(EIU)中，所有类型的白细胞都 出现在小鼠实验性眼睑炎中。细胞因子(例如， 淋巴因子)和炎症介质(如一氧化氮)发挥作用 在葡萄膜炎免疫发病机制中的重要作用。的表达 主要组织相容性(MHC)II类抗原和黏附分子 在炎症过程中观察到眼部驻留细胞。 我们研究了转化生长因子-β1(TGF-β1)，它是一种 调节啮齿动物EMIU、小鼠EIU和 转化生长因子-β1转基因小鼠。转化生长因子-β1通过抑制子宫肌瘤复发 将Th1细胞因子转变为Th2细胞因子。全身性转化生长因子-β1抑制EIU 血清IL-6水平。进行性白内障和一过性视网膜水肿 在转化生长因子-β1转基因小鼠体内发育。然而，没有显著的 在诱导EIU的过程中，我们发现了转基因之间的差异 老鼠和野生型的对照组。我们得出结论：转化生长因子-β1 通过复杂的细胞因子网络调节炎症，可能是 对治疗人类葡萄膜炎很有用。其他细胞因子和 炎症介质也可能对治疗有益。一氧化氮 保护眼睛免受弓形虫侵袭，限制免疫反应。 IL-12对EIU有抑制作用。 从患有各种疾病的人的眼睛组织中提取的样本，包括 葡萄膜炎、视网膜和角膜疾病、肿瘤和代谢遗传学 疾病，通过常规的组织学研究， 免疫组织化学和原位杂交技术。在葡萄膜炎中， 免疫活性细胞和细胞因子，以及刺激物 (例如，感染性生物)是进行临床研究的有价值的辅助工具 诊断和了解疾病的发病机制。高程 检测玻璃体中的IL-10有助于诊断眼内大B细胞 淋巴瘤，通常伪装成特发性葡萄膜炎。我们有 报道称，艾滋病患者会发生转移性脉络膜细菌性脓肿，以及 痤疮丙酸杆菌细胞壁结构增厚可能与 对寄主对细菌杀灭和降解的抗性 中性粒细胞和巨噬细胞。阐明其在免疫病理中的作用 眼部浸润性细胞与眼内停留细胞的关系 将帮助我们更好地了解和管理各种眼科疾病 病人中的疾病。

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 and in situ hybridization. Previously, we have demonstrated that T lymphocytes, in particular the CD4 cells, were the predominant infiltrating cells in experimental autoimmune uveoretinitis (EAU) and experimental melanin-protein induced uveitis (EMIU), yet both macrophages and polymorphonuclear neutrophils were the predominant infiltrating cells in endotoxin-induced uveitis (EIU) and all types of leukocytes were present in murine experimental blepharitis. Cytokines (e.g., lymphokines) and inflammatory mediators (e.g., nitric oxide) play an important role in the immunopathogenesis of uveitis. Expressions of major histocompatibility class (MHC) II antigens and adhesion molecules are observed on ocular resident cells during the inflammatory process. We have studied transforming growth factor-beta (TGF-beta1), one of the cytokines that modulates inflammation in rodent EMIU, murine EIU, and TGF-beta1 transgenic mice. TGF-beta1 inhibits the recurrence of EMIU by shifting Th1 to Th2 cytokine profile. Systemic TGF-beta1 suppresses EIU and serum IL-6 levels. Progressive cataract and transient retinal edema develop in TGF-beta1 transgenic mice. However, no significant differences in the induction of EIU were found between the transgenic mice and the wild-type controls. We have concluded that TGF-beta1 regulates inflammation through the complex cytokine network and may be useful for the treatment of human uveitis. Other cytokines and inflammatory mediators may also be beneficial for therapy. Nitric oxide protects against ocular Toxoplasma gondii and limits the immune response. IL-12 inhibits EIU. Specimens from human ocular tissues with various diseases, including uveitis, retinal and corneal diseases, tumors, and metabolic genetic disorders, are studied by using routine histological, immunohistochemical, and in situ hybridization techniques. In uveitis, immunocompetent cells and cytokines, in addition to the stimulators (e.g., infectious organisms), are valuable adjuncts for making a clinical diagnosis and understanding the pathogenesis of the diseases. Elevation of IL-10 in the vitreous helps to diagnose intraocular large B-cell lymphoma, which frequently masquerades as idiopathic uveitis. We have reported that metastatic choroidal bacterial abscess occurs in AIDS, and the thickened cell wall structure of Propionibacterium acnes may relate to the resistance of bacterial killing and degradation by the host neutrophils and macrophages. Elucidating the immunopathological role of the relationship between the infiltrating cells and ocular resident cells will help us gain a better understanding and management of various ocular diseases in patients.