Type I Interferon: Friend and Foe Alike

摘要 请求为题为“I型干扰素：朋友和敌人相同”的Keystone专题讨论会会议提供支助， 由Alan Sher、Virginia Pascual、Adolfo García-Sastre和Anne O 'Garra博士组织。会议将 2017年3月19日至23日在加拿大阿尔伯塔班夫举行。虽然细胞因子在宿主防御中起关键作用， 在免疫稳态中，它们在其他环境中可以是炎症病理学的关键介质。这一重要 功能性二分法可能在I型干扰素在健康中的不同活性中得到最好的例证， 疾病I型干扰素调节一个广泛的基因家族，这些基因刺激或抑制免疫功能， 对宿主有保护作用或有害作用。因此，虽然I型IFN因其抗病毒作用而众所周知， 活性和刺激效应T细胞应答，它们还可以促进自身免疫，细菌，甚至 某些病毒性疾病理解这种背景依赖性对于揭示 I型干扰素依赖性疾病和基于干扰素的治疗设计，将是中心的重点， 了那次会议本次会议将以演讲开始，介绍I型IFN基因及其 调节，先天识别机制和信号转导途径的I型干扰素诱导和孟德尔- 基于干扰素的疾病其他会议将集中在I型干扰素的作用，在病毒，细菌和 自身免疫性疾病会议最后将讨论机械因素和背景因素 确定I型IFN诱导的有益与有害结果以及这些信息如何 应用于靶向治疗干预的开发。由于该主题的及时性， 会议应吸引来自细胞因子生物学，炎症，传染病等领域的广泛观众 和转化医学，并吸引了坚实的行业代表。跨学科的机会 互动将显着增强并行会议模式识别信号：从 先天免疫炎症性疾病，这将分享一个主题演讲和全体会议与此 会议

ABSTRACT Support is requested for a Keystone Symposia meeting entitled Type I Interferon: Friend and Foe Alike, organized by Drs. Alan Sher, Virginia Pascual, Adolfo García-Sastre and Anne O'Garra. The meeting will be held in Banff, Alberta, Canada from March 19-23, 2017. While cytokines play critical roles in host defense and immune homeostasis, they in other settings can be key mediators of inflammatory pathology. This important functional dichotomy is perhaps best exemplified in the diverse activities of Type I interferon(s) in health and disease. Type I IFNs regulate a broad family of genes that either stimulate or inhibit immune function and in so doing have host protective or detrimental effects. Thus, while Type I IFNs are well-known for their anti-viral activity and stimulation of effector T cell responses, they can also promote autoimmune, bacterial and even certain viral diseases. Understanding this contextual dependency is crucial for unraveling the pathogenesis of Type I IFN-dependent diseases and for the design of interferon-based therapies and will be the central focus of the meeting. This conference will open with talks presenting an overview of Type I IFN genes and their regulation, innate recognition mechanisms and signaling pathways for Type I IFN induction and Mendelian- based interferonopathies. Additional sessions will focus on the role of Type I IFN in viral, bacterial and autoimmune diseases. The meeting will conclude with a discussion of the mechanistic and contextual factors that determine the beneficial versus deleterious outcome of Type I IFN induction and how this information can be applied to the development of targeted therapeutic interventions. Because of the timeliness of the topic, the conference should draw a broad audience from the fields of cytokine biology, inflammation, infectious disease and translational medicine and attract a solid industry representation. Opportunities for interdisciplinary interactions will be significantly enhanced by the concurrent meeting on Pattern Recognition Signaling: From Innate Immunity to Inflammatory Disease, which will share a keynote address and plenary session with this meeting.