CORE--IMMUNOLOGY

核心--免疫学

• 批准号: 6564372
• 负责人: Jerry R McGhee
• 金额: $ 16.54万
• 依托单位: UNIVERSITY OF ALABAMA AT BIRMINGHAM
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-01-01 至 2002-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6564372
• 关键词: T lymphocyte; biomedical facility; cytotoxic T lymphocyte; genetically modified animals; helper T lymphocyte; immunology; inflammation; laboratory mouse; leukocyte activation /transformation; mucosal immunity; transfection /expression vector

Description: (Taken directly from the application) In order to obtain a better understanding of the induced mucosal and systemic immune responses to both transgene and vector, the associated T cell subset responses which include CD4+, CD8+, alpha beta and gamma-delta T cells and mucosal antibody responses in the respiratory tract and systemic compartment will be analyzed in the Immunology Core. The activation of CD4+ T helper type 1 (Th1) cells for the induction of cell-mediated immunity (as manifested by delayed type hypersensitivity) which contribute to inflammation and antibody mediated immunity regulated by Th2-type helper cells will be analyzed in the respiratory tract and associated lymph nodes. The roles for key Th1 and Th2 cytokines like IFN-y and IL-4 for the induction of these two T helper cell subsets will be assessed by the use of cytokine gene disrupted (knockout) mice. This will contribute to our understanding of vector-specific immunity and may reveal pathways to specifically decrease these responses by the absence or over-expression of specific cytokines. In addition to Th1 and Th2 cells, it is also clear that gamma delta T cells can play an incompletely understood role in the mucosal immune response. Therefore, our studies in the Core will address their potential role in mucosal and systemic immunity to vector and transgene by assessing their contribution in normal and gamma delta TCR-deficient mice. This Immunology Core will provide state-of-the-art analyses of Th1- and Th2-type and CTL responses to various constructs developed by CF gene Therapy Core Center investigators and pilot projects. In so doing, we will help optimize the vector and transgene for effective therapy with minimum inflammation.

描述：（直接取自应用程序） 为了更好地了解诱导的粘膜和全身 对转基因和载体以及相关 T 细胞亚群的免疫反应 反应包括 CD4+、CD8+、αβ 和 γ-δ T 细胞以及 呼吸道和全身区室的粘膜抗体反应 将在免疫学核心中进行分析。 CD4+ T 辅助细胞 1 型的激活 (Th1) 细胞用于诱导细胞介导的免疫（如 迟发型超敏反应），这会导致炎症和抗体 Th2型辅助细胞介导的免疫调节将在 呼吸道和相关淋巴结。关键 Th1 和 Th2 的作用 IFN-y 和 IL-4 等细胞因子用于诱导这两种 T 辅助细胞 将通过使用细胞因子基因破坏（敲除）小鼠来评估子集。 这将有助于我们对载体特异性免疫的理解，并可能 揭示通过不存在或不存在来专门减少这些反应的途径 特定细胞因子的过度表达。除 Th1 和 Th2 细胞外， 还清楚地表明，γδT 细胞在 粘膜免疫反应。因此，我们的核心研究将解决 它们在载体和转基因的粘膜和全身免疫中的潜在作用 通过评估它们对正常和 γ δ TCR 缺陷小鼠的贡献。 该免疫学核心将提供最先进的 Th1 和 Th2 型和 CTL 对 CF 基因疗法开发的各种构建体的反应 核心中心研究人员和试点项目。这样做，我们将帮助 优化载体和转基因，以最小的成本实现有效的治疗 炎。