ROLE OF CHEMOKINES IN MUCOSAL IMMUNITY: ORAL, RESPIRATORY & UROGENITAL PATHOGENS

趋化因子在粘膜免疫中的作用：口腔、呼吸道

• 批准号: 7335986
• 负责人: James W Lillard
• 金额: $ 15.78万
• 依托单位: MOREHOUSE SCHOOL OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-06-01 至 2007-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7335986
• 关键词: chemokine; cytokine; immunity; mucosal immunity; role

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 first aim of this project will assess the mucosal and systemic immunity in mice defective in the production or recognition of chemokines following mucosal immunization with Th1- or Th2-inducing regimens. The second aim will determine the G protein(s) - dependent and -independent mechanisms that these chemokines use to enhance acquired immunity. The third aim will assess the role of CD28-B7 and CD40-CD40L interactions as well as B and T cell differentiation for antibody, T helper cytokine, and cytotoxic T cell responses that occur in chemokine-mediated adaptive immunity. The fourth aim will define the Th1- and Th2-type cytokine -dependent and -independent pathways that result when chemokines are administered with protein antigen through mucosal or systemic routes. The proposed studies will provide important and novel information regarding the cellular mechanisms that chemokines, RANTES, Lptn, IP-10, and IL-8 use to induce and regulate systemic and mucosal immunity.

该子项目是利用 NIH/NCRR 资助的中心拨款提供的资源的众多研究子项目之一。子项目和研究者 (PI) 可能已从另一个 NIH 来源获得主要资金，因此可以在其他 CRISP 条目中出现。列出的机构是中心的机构，不一定是研究者的机构。该项目的第一个目标是评估在使用 Th1 或 Th2 诱导方案进行粘膜免疫后趋化因子产生或识别有缺陷的小鼠的粘膜和全身免疫。第二个目标将确定这些趋化因子用于增强获得性免疫的 G 蛋白依赖性和非依赖性机制。第三个目标将评估 CD28-B7 和 CD40-CD40L 相互作用以及 B 细胞和 T 细胞分化对抗体、T 辅助细胞因子和趋化因子介导的适应性免疫中发生的细胞毒性 T 细胞反应的作用。第四个目标将定义 Th1 型和 Th2 型细胞因子依赖性和非依赖性途径，这些途径是通过粘膜或全身途径与蛋白质抗原一起施用趋化因子时产生的。拟议的研究将提供有关趋化因子、RANTES、Lptn、IP-10 和 IL-8 用于诱导和调节全身和粘膜免疫的细胞机制的重要且新颖的信息。