Regulating Interferon signalling in innate immunity

我们的先天免疫系统进化为对抗感染的前线防御。然而，不受控制的反应可能导致严重的疾病，如败血性休克、慢性炎症（如肝炎）、自身免疫性疾病（如系统性红斑狼疮）。免疫反应是由重要的激素，如干扰素，在这些情况下产生的身体调节。该项目旨在了解在不限制干扰素的积极或有益作用的情况下防止其危险副作用的消极或抑制机制。我们将研究一种称为细胞因子信号抑制因子1（socs1）的分子的作用，我们最近发现它可以调节小鼠中干扰素的作用。最初，我们的研究将确定SOCS1与细胞内的哪些分子结合，以及对细胞激活途径的影响。下一步将是在小鼠中特异性阻断这种相互作用，并确定对病毒感染和炎症疾病模型的影响。这些研究的结果将更好地了解人体如何通过免疫反应和潜在的新方法来开发治疗药物来对抗疾病。

Our innate immune system evolved as the front line defence against infection. However an uncontrolled response can lead to serious diseases such as septic shock, chronic inflammation as in hepatitis, autoimmune diseases such as systemic lupus erythematosus. The immune respnse is regulated by important hormones such as interferon produced by the body in these situations. This project aims to understand the negative or inhibitory mechanisms that prevent dangerous side effects of interferons without restricting their postive or beneficial effects. We will examine the actions of a molecule called the Suppressor of cytokin Signaling 1 (socs1) which we have recently discovered to modulate the actions of interferon in the mouse. Initially our studies will determine which molecules SOCS1 binds to inside a cell and the consequences for cell activation pathways. The next step will be to specifically block this interaction in the mouse and determine the effects on models of viral infection and inflammatory disease. The outcome of these studies will be a better understanding of how the body fights disease via the immune response and potential new approaches to develop therapeutic drugs.