Department of Viroscience, Erasmus MC, Rotterdam, Netherlands.
Front Immunol. 2019 Jul 25;10:1763. doi: 10.3389/fimmu.2019.01763. eCollection 2019.
Specialized receptors that recognize molecular patterns such as double stranded RNA duplexes-indicative of viral replication-are potent triggers of the innate immune system. Although their activation is beneficial during viral infection, RNA transcribed from endogenous mobile genetic elements may also act as ligands potentially causing autoimmunity. Recent advances indicate that the adenosine deaminase ADAR1 through RNA editing is involved in dampening the canonical antiviral RIG-I-like receptor-, PKR-, and OAS-RNAse L pathways to prevent autoimmunity. However, this inhibitory effect must be overcome during viral infections. In this review we discuss ADAR1's critical role in balancing immune activation and self-tolerance.
专门识别分子模式(如双链 RNA 双链)的受体 - 表明病毒复制 - 是先天免疫系统的有效触发因素。尽管它们的激活在病毒感染期间是有益的,但从内源性移动遗传元件转录的 RNA 也可能作为配体潜在地导致自身免疫。最近的进展表明,腺苷脱氨酶 ADAR1 通过 RNA 编辑参与抑制经典抗病毒 RIG-I 样受体 - PKR - 和 OAS-RNAse L 途径,以防止自身免疫。然而,这种抑制作用必须在病毒感染期间克服。在这篇综述中,我们讨论了 ADAR1 在平衡免疫激活和自身耐受方面的关键作用。