IMMUNOMODULATION DURING PULMONARY CRYPTOCOCCOSIS

隐球菌病是一种真菌病， 无处不在的酵母样生物，新型隐球菌。的 原发性肺部疾病的范围可以从轻度到重度， 宿主的免疫状态 目标是确定 抗隐球菌反应下降的机制 监管. 具体目的是：1）评估IL-10和IL-10在肿瘤细胞中的作用。 4下调小鼠抗隐球菌CMI反应 感染C. 新生儿分离物NU-2或184 A; 2）检查 TGF-β和TNF α时间分布图，并确定是否阻断 这些细胞因子中的一种或两种的活性将改变细胞的免疫功能。 抗隐球菌CMI反应; 3）确定白细胞表面 标记物如B7-1、B7-2、主要组织相容性复合体（MHC） 抗原呈递细胞和CD 28上的II类抗原（1-A和I-E） CD 4+和CD 8 + T淋巴细胞上的CTLA-4被调节 并研究这些变化对促进 NU-2感染小鼠中抗隐球菌CMI反应的偏差; 4)检测Fas/FasL介导的凋亡在细胞凋亡中的作用， NU-2感染者中抗隐球菌CMI反应的调节 小鼠; 5）应用差异显示聚合酶链反应 （DD-PCR）技术来建立由 NU-2感染（调节的CMI反应）与 由184 A（延长的保护性CMI）感染诱导的mRNA 在小鼠模型中。

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.