Mechanisms of immune homeostasis and regulation of intraocular inflammation

免疫稳态机制和眼内炎症调节

• 批准号: 9155560
• 负责人: Charles E Egwuagu
• 金额: $ 29.85万
• 依托单位: NATIONAL EYE INSTITUTE
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/9155560
• 关键词: Activated Lymphocyte; Area; Autoimmune Diseases; Autoimmune Process; B-Lymphocytes; Biologic Development; Biology; CD8-Positive T-Lymphocytes; CISH gene; Cell Death; Cell Proliferation; Cells; Chronic; Communicable Diseases; Development; Disease; Embryonic Development; Epigenetic Process; Etiology; Goals; Homeostasis; IFN consensus sequence binding protein; Immune; Immune system; Immunity; Inflammation; Inflammatory; Insecta; Interleukins; Lymphocyte; Mammals; Neurodegenerative Disorders; PTPN6 gene; Pathogenesis; Pathologic; Pathway interactions; Physarum polycephalum; Physiological Processes; Play; Regulation; Research; Retinal Degeneration; Role; STAT3 gene; Signal Pathway; Signal Transduction; Signal Transduction Pathway; T-Lymphocyte; T-Lymphocyte Subsets; Uveitis; adaptive immunity; base; cytokine; interest; protein inhibitors of activated STAT

Our research focused on 3 broad themes: (i) Etiology and pathogenesis of ocular inflammatory diseases. (ii) Development of Biologics for treating autoimmune diseases; (iii) T cell and cytokine biology: Contributions to basic mechanisms of host immunity. Significant advances in each of these areas include: 1. Discovery that Interleukin-35 induces regulatory B cells that suppress autoimmune disease. 2. Characterization of factors that underlie the development of chronic intraocular inflammation and retinal degenerative disease. (3) Demonstration of the critical roles of IRF-8, STAT3, SOCS1, cytokines in the development and suppression uveitis.

我们的研究集中在三个广泛的主题上：（i）眼部炎症性疾病的病因和发病机理。 （ii）开发用于治疗自身免疫性疾病的生物制剂； （iii）T细胞和细胞因子生物学：对宿主免疫基本机制的贡献。这些领域的每个领域都取得了重大进展： 1。发现白介素-35诱导抑制自身免疫性疾病的调节B细胞。 2。表征慢性眼内炎症和视网膜退行性疾病的因素的表征。 （3）证明IRF-8，STAT3，SOCS1，细胞因子在发育和抑制葡萄膜炎中的关键作用。