LYMPHOKINES, CELLULAR IMMUNITY, DELAYED HYPERSENSITIVITY

淋巴因子、细胞免疫、迟发性超敏反应

• 批准号: 3179237
• 负责人: SAMUEL B SALVIN
• 金额: $ 11.8万
• 依托单位: UNIVERSITY OF PITTSBURGH AT PITTSBURGH
• 依托单位国家: 美国
• 财政年份: 1985
• 资助国家: 美国
• 起止时间: 1985-01-01 至 1987-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3179237
• 关键词: Candida albicans; Escherichia coli; Mycobacterium bovis; T lymphocyte; bacterial antigens; cell type; delayed hypersensitivity; fungal antigens; genetic strain; hormone regulation /control mechanism; lymph nodes; lymphokines; messenger RNA; microorganism immunology; molecular cloning; spleen; tissue /cell culture

The primary aim is to determine the interrelationship between: (1) cell-mediated immunity (CMI); (2) in vivo release of migration inhibitory factor (MIF) and/or interferon-gamma (IFN-gamma); and (3) delayed hypersensitivity. The studies will be carried out in two types of inbred mice: (1) those resistant to Candida albicans and Mycobacterium bovis (BCG), high responders (in the in vivo release of the two lymphokines, MIF and IFN), and good reactors in delayed hypersensitivity; and (2) those susceptible to infection with C. albicans, low responders in in vivo MIF, and poor reactors in delayed hypersensitivity. Experiments will be planned and run to isolate the messenger RNAs involved in the formation or development of the three aforementioned immunologic phenomena. The messenger RNA fractions coding for MIF or a related factor causing cell-mediated immunity will be purified. The cDNA will be prepared and the responsible gene(s) isolated by molecular cloning in E. coli. Such clones will then be used for the production of MIF of the factor(s) causing cell-mediated immunity. These purified factors will then be analyzed for their capacity to enhance CMI in the susceptible murine strains. The cells responsible for the formation of the lymphokines and for the development of cell-mediated immunity will be separated and characterized. Also the thymic peptides that enhance or suppress CMI will be determined and the particular cellular circuits that they effect will be analyzed. (HF)

主要目的是确定以下方面之间的相互关系：（1） 细胞介导的免疫（CMI）;（2）体内释放迁移抑制剂 因子（MIF）和/或干扰素-γ（IFN-γ）;和（3）延迟 超敏反应 研究将在两种类型的近交系中进行 小鼠：（1）白色念珠菌和牛分枝杆菌耐药小鼠 (BCG)高反应者（在体内释放两种淋巴因子，MIF 和IFN），以及迟发型超敏反应良好的反应者;和（2）那些 易感染C.白色念珠菌，体内MIF低应答者， 迟发型超敏反应差。 将计划进行实验 并分离出参与形成的信使RNA 上述三种免疫现象的发生。 的 编码MIF或相关因子的信使RNA片段， 细胞介导的免疫将被纯化。 将制备cDNA， 在E.杆菌 这些克隆 然后将用于产生导致 细胞免疫 然后将分析这些纯化的因子， 它们增强易感鼠品系中CMI的能力。 细胞 负责淋巴因子的形成和 细胞介导的免疫将被分离和表征。 也 将测定增强或抑制CMI的胸腺肽， 将分析它们影响的特定细胞回路。 （HF）