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IMMUNOMODULATION DURING PULMONARY CRYPTOCOCCOSIS

肺隐球菌病期间的免疫调节

基本信息

批准号：
6389843
负责人：
JUNEANN W MURPHY
金额：
$ 25.55万
依托单位：
UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR
依托单位国家：
美国
项目类别：
财政年份：
1997
资助国家：
美国
起止时间：
1997-09-30 至 2003-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/6389843
关键词：
CD28 molecule CD95 molecule Cryptococcus neoformans MHC class II antigen T lymphocyte antigen presenting cell apoptosis cellular immunity cryptococcosis cytokine immunoregulation interleukin 10 interleukin 4 laboratory mouse microorganism immunology polymerase chain reaction transforming growth factors tumor necrosis factor alpha

项目摘要

Cryptococcosis is a mycotic disease that is acquired by inhalation of the ubiquitous yeast-like organism, Cryptococcus neoformans. The primary pulmonary disease can range from mild to severe depending on the host's immunological status. The goal is to identify the mechanisms by which the anticryptococcal responses are down- regulated. The specific aims are: 1) to assess the role of IL-10 and IL- 4 in down-regulation of the anticryptococcal CMI response in mice infected with C. neoformans isolate NU-2 or 184A; 2) to examine the temporal profile of TGF-beta and TNFalpha and determine if blocking the activity of either or both of these cytokines would alter the anticryptococcal CMI response; 3) to determine if leukocyte surface markers such as B7-1, B7-2, major histocompatibility complex (MHC) class II antigens (1-A and I-E) on antigen presenting cells and CD28 and CTLA-4 on CD4plus and CD8plus T lymphocytes are modulated and examine the potential for the changes to contribute to the deviation in the anticryptococcal CMI response in NU-2-infected mice; 4) to examine the role of Fas/FasL-mediated apoptosis in the regulation of the anticryptococcal CMI response in the NU-2 infected mice; and 5) to apply differential display polymerase chain reaction (DD-PCR) technology to establish differences in mRNAs inducted by an infection with NU-2 (modulated CMI response) compared to mRNAs induced by an infection with 184A (prolonged protective CMI response) in the mouse model.

隐球菌病是一种真菌性疾病，通过吸入无处不在的类酵母生物，新型隐球菌。这原发性肺部疾病的范围可以从轻微到严重，具体取决于与宿主的免疫状态有关。目标是确定抗隐球菌反应下降的机制受监管。具体目标是： 1) 评估 IL-10 和 IL-10 的作用 4 下调小鼠抗隐球菌 CMI 反应感染新型隐球菌分离株 NU-2 或 184A； 2）检查 TGF-β 和 TNFα 的时间分布并确定是否阻断这些细胞因子中的任何一种或两种的活性都会改变抗隐球菌 CMI 反应； 3) 判断白细胞表面是否标记物，例如 B7-1、B7-2、主要组织相容性复合体 (MHC) 抗原呈递细胞和 CD28 上的 II 类抗原（1-A 和 I-E） CD4+ 和 CD8+ T 淋巴细胞上的 CTLA-4 受到调节并检查变革对促进变革的潜力 NU-2 感染小鼠的抗隐球菌 CMI 反应出现偏差； 4) 研究Fas/FasL介导的细胞凋亡在细胞凋亡中的作用 NU-2感染者抗隐球菌CMI反应的调节老鼠； 5)应用差异显示聚合酶链式反应 (DD-PCR) 技术来确定 mRNA 的差异与 NU-2 感染（调节 CMI 反应）相比 184A 感染诱导的 mRNA（长期保护性 CMI）响应）在小鼠模型中。