CCR7 Chemotaxis Regulates Memory T Cell Localization

当人类暴露于一种引起免疫反应的物质时，为了保护自身， 身体会产生抗体关于趋化因子在调节细胞凋亡中的作用， 免疫反应的程度，通过抗体滴度和抗体类型来衡量。我们 已经发现C-C趋化因子受体7通过控制C-C趋化因子的定位来调节抗体滴度。 不同的免疫细胞群进入骨髓。在本提案中，我们的目标是更好地了解 免疫T细胞应答C-C趋化因子受体7的分子机制 激活调节T细胞靶向骨髓，在那里它们调节同种型转换 以及免疫细胞产生抗体。我们的研究是重要的，因为这些抗体保护宿主， 他或她在二次免疫反应期间暴露于相同的物质。我们假设 CCR 7调节记忆性T细胞和调节性T细胞向骨髓的迁移，以限制记忆性T细胞的激活。 B细胞在适应性免疫反应中。随着知识的积累，我们将决定是否重定向 T细胞可用于抑制在自身免疫疾病期间观察到的过度免疫应答。

ABSTRACT When humans are exposed to a substance that causes an immune response, to protect the itself, the body generates antibodies. There is very little understood about the role of chemokines in regulating the extent of the immune response, as measured by antibody titers and types of antibodies that are made. We have found that C-C chemokine receptor 7 regulates the antibody titers by controlling the localization of different populations of immune cells to the bone marrow. In this proposal our goal is to better understand the molecular mechanisms that are employed by immune T cells to respond to C-C chemokine receptor 7 activation that regulate the targeting of T cells to the bone marrow where they regulate the isotype switching and antibody production by immune cells. Our study is important since these antibodies protect the host when he or she is exposed to the same substance during a secondary immune response. We hypothesize that CCR7 regulates the migration of memory T, and regulatory T cells to the bone marrow to limit the activation of B cells during an adaptive immune response. With the knowledge we gain we will determine if redirection of the T cells can be applied to inhibit excessive immune responses observed during autoimmune diseases.