KIR AND MHC CLASS I IMMUNOGENETICS IN SIV INFECTION

SIV 感染中的 KIR 和 MHC I 类免疫遗传学

• 批准号: 8357992
• 负责人: David T Evans
• 金额: $ 21.06万
• 依托单位: HARVARD MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-05-01 至 2012-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8357992
• 关键词: Animal Experiments; Disease Progression; Funding; Genetic; Genetic Polymorphism; Grant; HIV-1; Histocompatibility Antigens Class I; Immunogenetics; Individual; Infection; Ligands; MHC Class I Genes; Macaca mulatta; National Center for Research Resources; Natural Killer Cells; New England; Play; Primates; Principal Investigator; Regulation; Research; Research Infrastructure; Resources; Role; SIV; Source; United States National Institutes of Health; base; cost; design; response

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Genetic evidence indicates that KIR and HLA class I polymorphisms play an important role in determining the rate of disease progression in HIV-1 infected individuals. However, the immunological mechanisms underlying these observations are poorly understood. We recently identified Mamu-A1*00201 (Mamu-A*02), a common MHC class I molecule in the rhesus macaque, as a ligand for Mamu-KIR3DL05. Using KIR- and MHC class I-defined animals, experiments can now be designed to examine the role of this KIR-MHC class I interaction in the regulation of NK cell responses to SIV infection.

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 遗传学证据表明，KIR和HLA I类多态性在决定HIV-1感染者疾病进展速度方面发挥重要作用。然而，这些观察结果背后的免疫学机制知之甚少。我们最近鉴定了Mamu-A1 * 00201（Mamu-A * 02），一种恒河猴中常见的MHC I类分子，作为Mamu-KIR3DL05的配体。使用KIR和MHC I类定义的动物，现在可以设计实验来检查这种KIR-MHC I类相互作用在调节NK细胞对SIV感染的反应中的作用。