加速I型干扰素病：I型干扰素抗病毒应答的调节和功能

StephenW

Fueling Type I Interferonopathies: Regulation and Function of Type I Interferon Antiviral Responses

Chen Seng Ng
, Hiroki Kato
, and Takashi Fujita
Published Online: 8 Jul 2019https://doi.org/10.1089/jir.2019.0037

   
Abstract

In conjunction with the development of genome-wide technology, numerous studies have revealed the importance of regulatory mechanisms to avoid the onset of autoimmunity. In this, protein regulators and the newly identified low-abundant RNA species participate in the regulation of type I interferon ( IFN-I) and proinflammatory genes induced by innate immune sensors. In this review, we brief look into some of the autoimmune diseases profiled by dysregulations of IFN-I signaling and the regulatory channels critical for immunological homeostasis.
Introduction

Type I interferon (IFN-I) responses serve as the first line of host defense against microbe invasion. In response to infection, germline encoded pattern-recognition receptors (PRRs), including Toll-like receptors (TLRs), RIG-I-like </ RTI> </ RTI> <RTIgt; PRR induces IFN-I, including IFN-α and IFN-β, produced ubiquitously in different tissues, dendritic cells (DCs) and macrophages. Secondarily, IFN-I exerts various immune responses through recognition of its cognate receptors on target cells and results in Modulation of diverse processes such as antigen presentation and activation of adaptive immunological process involving B and T cells. Transcriptional control of IFN-I production and recreation induction of hundreds of products collectively Invasive control, cells possess mechanisms targeting signaling by positive and negative regulators of transcription In the case of IFN-I induction and its regulation to help us understand the onset and development of autoimmunity, termed type I interferonopathies.

StephenW

加速I型干扰素病：I型干扰素抗病毒应答的调节和功能

陈胜恩
，Hiroki Kato
和藤田隆
在线发布：2017年7月8日https：//doi.org/10.1089/jir.2019.0037


抽象

结合全基因组技术的发展，许多研究揭示了调节机制对于避免自身免疫发生的重要性。在此，蛋白质调节剂和新鉴定的低丰度RNA种类参与由先天免疫传感器诱导的I型干扰素（IFN-1）和促炎基因的调节。在这篇综述中，我们简要介绍一些自身免疫性疾病，这些疾病是由IFN-1信号传导的调节异常和对免疫稳态至关重要的调节通道所描述的。
介绍

I型干扰素（IFN-I）反应作为抵抗微生物入侵的宿主防御的第一线。响应于感染，种系编码的模式识别受体（PRR），包括Toll样受体（TLR），RIG-I样受体。 PRR诱导IFN-1，包括在不同组织，树突细胞（DC）和巨噬细胞中普遍产生的IFN-α和IFN-β。其次，IFN-1通过识别其在靶细胞上的同源受体而发挥各种免疫应答，并导致多种过程的调节，例如抗原呈递和涉及B和T细胞的适应性免疫过程的激活。转录控制IFN-1的产生和数百种产品的娱乐诱导共同侵袭性控制，细胞具有靶向转录阳性和阴性调节因子信号传导的机制在IFN-1诱导及其调节的情况下，帮助我们了解其发病和发展自身免疫，称为I型干扰素病。

StephenW

https://www.liebertpub.com/doi/1 ... &mcid=558087280