REGULATION OF CCR7 MEDIATED ADHESION OF T CELLS THROUGH LFA-1

通过 LFA-1 调节 CCR7 介导的 T 细胞粘附

• 批准号: 7381287
• 负责人: CHARLOTTE M VINES
• 金额: $ 16.34万
• 依托单位: UNIVERSITY OF KANSAS MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-07-27 至 2007-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7381287
• 关键词: adhesions; proteins

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. When our bodies are infected with viruses and different diseases our immune systems instruct T cells to fight each new infection. To make T cells that are needed to fight infections, the T cells must leave the blood stream and travel to areas where they can learn about new viruses or organisms that are invading the body. These areas are called lymph nodes. To reach the lymph nodes T cells must become sticky by turning on adhesion proteins and flatten to be able to move while fluid is flowing around them. The T cells express a protein on their surface, CCR7, which tells the cell?s adhesion proteins where the T cell needs to adhere, to defend the body against disease. Only un-instructed (na¿ve) T cells, which express high levels of CCR7, can fight new invasions. There are two different proteins that turn on CCR7 signaling by binding to CCR7, which are called CCL19 and CCL21. How CCR7 communicates with the cell?s adhesion proteins in response to binding to CCL19 or CCL21 is unclear. In our study we are beginning to learn what events take place inside T cells that turn on adhesion, by stimulating CCR7 with either CCL19 or CCL21 and measuring cell adhesion or cell spreading (flattening). We will identify proteins, by Western Blotting, that turn on adhesion in T-cells after binding to either CCL19 and/or CCL21. These studies will provide a better understanding of the role of CCR7 in T cell adhesion.

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 条目中得到体现。列出的机构是中心的机构，不一定是研究者的机构。当我们的身体感染病毒和不同疾病时，我们的免疫系统会指示 T 细胞对抗每种新的感染。为了制造抵抗感染所需的 T 细胞，T 细胞必须离开血流并前往它们可以了解入侵身体的新病毒或生物体的区域。这些区域称为淋巴结。为了到达淋巴结，T 细胞必须通过打开粘附蛋白而变得粘稠，并变平，以便在液体在其周围流动时能够移动。 T 细胞在其表面表达一种蛋白质 CCR7，它告诉细胞的粘附蛋白 T 细胞需要粘附在哪里，以保护身体免受疾病侵害。只有表达高水平 CCR7 的未经指导的（原始）T 细胞才能抵抗新的入侵。有两种不同的蛋白质通过与 CCR7 结合来开启 CCR7 信号传导，分别称为 CCL19 和 CCL21。 CCR7 如何响应与 CCL19 或 CCL21 的结合而与细胞粘附蛋白进行通信尚不清楚。在我们的研究中，我们开始通过用 CCL19 或 CCL21 刺激 CCR7 并测量细胞粘附或细胞扩散（扁平化）来了解 T 细胞内部发生哪些事件来开启粘附。我们将通过蛋白质印迹鉴定与 CCL19 和/或 CCL21 结合后在 T 细胞中开启粘附的蛋白质。这些研究将有助于更好地了解 CCR7 在 T 细胞粘附中的作用。