驱动 I 型干扰素病：I 型干扰素抗病毒反应的调控与功能。
Fueling Type I Interferonopathies: Regulation and Function of Type I Interferon Antiviral Responses.
机构信息
1 Institute for Quantitative and Computational Biosciences, Immunology and Molecular Genetics, University of California, Los Angeles, California.
2 Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, California.
出版信息
J Interferon Cytokine Res. 2019 Jul;39(7):383-392. doi: 10.1089/jir.2019.0037. Epub 2019 Mar 21.
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 briefly look into some of the autoimmune diseases profiled by dysregulations of IFN-I signaling and the regulatory mechanisms critical for immunological homeostasis.
伴随着全基因组技术的发展，大量研究揭示了调控机制在避免自身免疫病发生中的重要性。在这一过程中，蛋白质调控因子和新发现的低丰度 RNA 种类参与了 I 型干扰素（IFN-I）和先天免疫传感器诱导的促炎基因的调控。在这篇综述中，我们简要探讨了一些由 IFN-I 信号转导失调和免疫稳态关键调控机制所导致的自身免疫病。
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