IMMUNE RESPONSE TO LEISHMANIA MAJOR

对大型利什曼原虫的免疫反应

• 批准号: 6169619
• 负责人: RICHARD GRAEME TITUS
• 金额: $ 29.97万
• 依托单位: COLORADO STATE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1993
• 资助国家: 美国
• 起止时间: 1993-04-01 至 2002-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6169619
• 关键词: B lymphocyte; CD40 molecule; Leishmania major; MHC class I antigen; T lymphocyte; antigen presenting cell; cellular immunity; cellular pathology; colony stimulating factor; genetically modified animals; host organism interaction; immunoregulation; in situ hybridization; interleukin 6; intracellular parasitism; laboratory mouse; leishmaniasis; leukocyte activation /transformation; molecular pathology; monokines; polymerase chain reaction; prostaglandin E; protozoal antigen; receptor expression; tissue /cell culture

DESCRIPTION (Adapted from the Applicant's Abstract): Following infection with Leishmania major (Lm), there is outgrowth of Th1 cells in mice that resolve the infection, but outgrowth of Th2 cell in mice that succumb to disease. This project will test 3 major subhypotheses: 1) To test the hypothesis that differential expression of MHC (I-A/E) and/or accessory (ICAM), LFA/co-stimulatory molecules (B7, CD40) by APCs and the secretion of monokines/factors by A{Cs influences Lm specific Th priming syngereic system; 2) to examine congenic/chimeric combinations of APCs and responding T cells to further test the hypothesis that APCs influence Th priming and to test additional hypothesis; 3) to monitor the expression of APC molecules important to T cell priming in cutaneous lesions of Lm and in the lymph nodes draining the lesion, and to test the hypothesis that factors that influence or are secreted by APCs (e.g., monokines, prostaglandin E2 (PGE2) affect Lm specific Th priming and the outcome of infection with Lm.

描述（改编自申请人摘要）：感染后 与硕大利什曼原虫（Lm）一起，在小鼠中存在Th 1细胞的生长， 解决感染，但Th 2细胞在小鼠中的生长， 疾病 本项目将测试3个主要的子假设：1）为了测试 MHC（I-A/E）和/或辅助分子差异表达假说 APCs对细胞间粘附分子（ICAM）、LFA/共刺激分子（B7、CD 40）的影响以及APCs分泌LFA/共刺激分子（B7、CD 40）的作用。 单核因子/因子通过A{Cs}影响Lm特异性Th启动协同效应 系统; 2）检查APC的同源/嵌合组合和应答 T细胞，以进一步检验APC影响Th引发的假设， 测试额外的假设; 3）监测APC分子的表达 对Lm皮肤病变和淋巴中的T细胞启动很重要 淋巴结引流病变，并测试假设的因素， 影响APC或由APC分泌（例如，单核因子，前列腺素E2（PGE 2） 影响Lm特异性Th引发和Lm感染的结果。