MECHANISMS OF T CELL ESCAPE BY ORTHOPOXVIRUSES

正痘病毒 T 细胞逃逸机制

• 批准号: 8173246
• 负责人: Klaus J Fruh
• 金额: $ 7.61万
• 依托单位: OREGON HEALTH & SCIENCE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2011-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8173246
• 关键词: APC Vaccine; Antigen-Presenting Cells; CD4 Positive T Lymphocytes; CD8B1 gene; Cells; Computer Retrieval of Information on Scientific Projects Database; Cowpox virus; Data; Disease Outbreaks; Funding; Genome; Goals; Grant; Homologous Gene; Immune; Immunomodulators; In Vitro; Individual; Infection; Institution; Monkeypox virus; Orthopoxvirus; Proteins; Publishing; Research; Research Personnel; Resources; Role; Source; T cell response; T-Lymphocyte; United States National Institutes of Health; Vaccinia virus; Viral; Virulence; prevent

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The longterm goal of this study is to understand the role of viral immune modulators for monkeypox virus (MPV) and cowpox virus (CPV) virulence. Individuals infected with MPV during the 2003 outbreak developed a strong MPV-specific T cell response, but the MPV-specific T cells were not stimulated by MPV-infected antigen presenting cells (APC) in vitro . In contrast, infection of APC by the vaccine strain Vaccinia-virus (VV) WR activated cross-reactive CD8+ and CD4+ T cells from MPV-infected individuals. These data strongly suggest that MPV prevents T cell stimulation by expressing immunomodulators that are absent in VV. Similarly, we observed that CPV-infected cells did not stimulate T cells. We succeeded in identifying the gene products of CPV that are responsible for T cell evasion. The results were recently published . We are currently evaluating homologous genes in the MPV-genome for their ability to inhibit T cell stimulation.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 这项研究的长期目标是了解病毒免疫调节剂在猴蛋白实病毒（MPV）和牛体病毒（CPV）毒力方面的作用。在2003年爆发期间感染了MPV的个体会产生强大的MPV特异性T细胞反应，但是在体外，MPV感染的抗原呈递细胞（APC）未刺激MPV特异性T细胞。相反，来自MPV感染的个体的疫苗菌株疫苗病毒（VV）WR感染APC。这些数据强烈表明MPV通过表达VV中不存在的免疫调节剂来阻止T细胞刺激。同样，我们观察到CPV感染的细胞没有刺激T细胞。 我们成功地识别了负责T细胞的CPV的基因产物。结果最近发表了。我们目前正在评估MPV基因组中的同源基因，以抑制T细胞刺激的能力。