The cyclic GMP-AMP synthase (cGAS)- Stimulator of Interferon Genes (STING) pathway of cytosolic DNA sensing allows mammalian cells to detect and respond to infection with diverse pathogens. Pathogens in turn encode numerous factors that inhibit nearly all steps of cGAS-STING signal transduction. From masking of cytosolic DNA ligands, to post-translational modification of cGAS and STING, and degradation of the nucleotide second messenger 2'3'-cGAMP, pathogens have evolved convergent mechanisms to evade cGAS-STING sensing. Here we examine pathogen inhibitors of innate immunity in the context of newly discovered regulatory features controlling cellular cGAS-STING activation. Comparative analysis of these strategies provides insight into mechanisms of action and suggests aspects of cGAS-STING regulation and immune evasion that remain to be discovered.

中文翻译：

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病原体逃避 cGAS-STING 免疫的保守策略。

环 GMP-AMP 合酶 (cGAS) - 细胞溶质 DNA 传感的干扰素基因刺激剂 (STING) 途径使哺乳动物细胞能够检测和应对不同病原体的感染。病原体反过来编码了许多抑制 cGAS-STING 信号转导的几乎所有步骤的因子。从胞质 DNA 配体的掩蔽，到 cGAS 和 STING 的翻译后修饰，以及核苷酸第二信使 2'3'-cGAMP 的降解，病原体已经进化出收敛机制来逃避 cGAS-STING 传感。在这里，我们在新发现的控制细胞 cGAS-STING 激活的调节特征的背景下检查了先天免疫的病原体抑制剂。