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.作者: StephenW 时间: 2019-7-20 13:28