CCL19 Regulation of the Secondary Immune Response

 描述(申请人提供)：当宿主(人或动物)接触到一种引起免疫反应的物质时，在某些情况下，身体会产生抗体。虽然产生保护性抗体是疫苗接种的目的，但人们对趋化因子在控制二次免疫反应期间产生的抗体的数量和类型方面的作用知之甚少。C-C趋化因子受体7是一种趋化因子受体，调节产生的抗体水平。我们研究的目标是了解宿主如何使用C-C趋化因子受体7来调节二次免疫反应期间产生的抗体水平。这一点很重要，因为在二次免疫反应期间，当宿主暴露在同一物质中时，抗体为宿主提供保护。我们假设，CCR7的丢失或向下游效应器(如ERK5)发出的信号将扰乱效应器记忆T细胞的靶向，导致第二次接触抗原后抗体产生增加。随着我们获得的知识，我们将确定在针对特定自身抗原的疫苗接种期间促进CCR7信号传递是否可以用于防止在自身免疫性疾病期间观察到的抗体的过度产生。

 DESCRIPTION (provided by applicant): When a host (person or animal) is exposed to a substance that causes an immune response, under certain circumstances the body generates antibodies. Although the generation of protective antibodies is the purpose of vaccinations, there is very little understood about the role of chemokines in controlling the numbers and types of antibodies that are produced during the secondary immune response. C-C chemokine receptor 7 is a chemokine receptor that regulates the levels of antibodies made. The goal of our studies is to learn how a host uses C-C chemokine receptor 7 to regulate the levels of antibodies that are made during a secondary immune response. This is important since antibodies provide protection to the host when he/she is exposed to the same substance during a secondary immune response. We hypothesize that loss of CCR7 or signaling to downstream effectors such as ERK5 will disrupt targeting of effector memory T cells leading to increased antibody production following the second exposure to an antigen. With the knowledge we gain we will determine if promoting CCR7 signaling during vaccination against a specific self-antigen, and in the near future, can be used to prevent excessive production of antibodies observed during autoimmune disease.