CELLULAR IMMUNITY TO CRYPTOSPORIDIUM PARVUM

描述（改编自申请人摘要）：研究者 提出了一种假设，即CD 40 L与活化的T细胞的结合 感染上皮细胞上的CD 40+有助于免疫 胆道系统和肠道中的微小隐孢子虫（Cp）。 的 研究者建议研究CD 40-CD 40 L 相互作用有助于Cp免疫，通过确定是否：1. CD40L 是Cp特异性免疫的传入或传出肢所必需的， 将Cp免疫和非免疫细胞转移到Cp感染的MHC匹配的 淘汰赛获奖者 2. γ-IFN、TNFR和/或IL的完整基因 12是Cp感染小鼠胆管硬化所必需的。 3. 的 Bcl-系列蛋白质的合成在细胞特异性基础上被抑制， Cp感染。 如果研究者证明Cp可以从 通过非特异性以及特异性T细胞介导胆管树 反应，随后在艾滋病患者的临床研究，使用 判别分析，将计划。

DESCRIPTION (Adapted from the Applicant's Abstract): The investigator proposes to test the hypothesis that binding of CD40L on activated T cells to CD40+ on infected epithelial cells contributes to immunity against Cryptosporidium parvum (Cp) in the biliary tree and the intestine. The investigator proposes to investigate the mechanisms by which CD40-CD40L interactions contribute to Cp immunity by determining whether: 1. CD40L is required for the afferent or efferent limb of Cp specific immunity by transfers of Cp immune and non-immune cells into Cp infected MHC matched knockout recipients. 2. The intact genes for gamma-IFN, TNFR, and/or IL 12 are required for sclerosis of bile ducts in Cp infected mice. 3. The synthesis of Bcl-series proteins is inhibited on a cell-specific basis by Cp infection. If the investigator shows that Cp can be eliminated from the biliary tree by non-specific as well as specific T-cell mediated responses, a subsequent clinical study in AIDS patients, using discriminant analysis, would be planned.