REGULATION OF CCR7 MEDIATED ADHESION OF T CELLS THROUGH LFA-1
REGULATION OF CCR7 MEDIATED ADHESION OF T CELLS THROUGH LFA-1
批准号:
7381287
负责人:
CHARLOTTE M VINES
金额:
$16.34万
依托单位国家:
美国
项目类别:
财政年份:
2006
资助国家:
美国
项目状态:
已结题
起止时间:
2006-07-27 至 2007-06-30
中文摘要
本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者(PI)可能已经从另一个NIH来源获得了主要资金,因此可以在其他CRISP条目中表示。列出的机构是中心的,不一定是研究者的机构。当我们的身体感染了病毒和不同的疾病时,我们的免疫系统会指示T细胞对抗每一种新的感染。为了制造对抗感染所需的T细胞,T细胞必须离开血流,前往能够了解正在入侵人体的新病毒或有机体的地方。这些区域被称为淋巴结。为了到达淋巴结,T细胞必须通过激活黏附蛋白而变得粘稠,当液体在它们周围流动时,T细胞必须变平才能移动。T细胞在其表面表达一种叫做CCR7的蛋白质,它告诉细胞?T细胞需要附着的黏附蛋白,以保护身体免受疾病的侵害。只有表达高水平CCR7的非指示(na - ve) 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,它们被称为CCL19和CCL21。CCR7如何与细胞沟通?在CCL19或CCL21结合时,s粘附蛋白的反应尚不清楚。在我们的研究中,通过用CCL19或CCL21刺激CCR7并测量细胞粘附或细胞扩散(变平),我们开始了解T细胞内部发生了什么事件,从而开启了粘附。我们将通过Western Blotting鉴定与CCL19和/或CCL21结合后在t细胞中开启粘附的蛋白。这些研究将更好地理解CCR7在T细胞粘附中的作用。
英文摘要
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.
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