The innate immune system serves as the first line of defense to protect the host from pathogen infection. As a first step, the pattern recognition receptors (PRRs) recognize pathogen-associated molecular patterns (PAMPs), such as non-self DNA derived from pathogens, and damage-associated molecular patterns (DAMPs), such as self DNA released from damaged or injured cells. Sensing of such DNAs elicits innate immune responses through the production of type I interferons (IFNs) and proinflammatory cytokines resulting from the activation of interferon regulatory factor 3 (IRF3) and nuclear factor kappa B (NF-κB), respectively. These cytokines are key players in interlinking innate and adaptive immune responses. However, defects in DNA sensors and their signaling cascades lead to dysregulation of immune responses, autoimmune diseases, and cancer progression. Here we provide an update on DNA signaling pathways in response to pathogen infection and cell injury, and on the roles of regulators in governing the immune system and maintaining host homeostasis. We also discuss the evasion of immunosurveillance by pathogens.

中文翻译：

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通过先天免疫受体及其信号传导途径感知自我和非自我DNA。

先天免疫系统是保护宿主免受病原体感染的第一道防线。第一步，模式识别受体（PRR）识别与病原体相关的分子模式（PAMP），例如源自病原体的非自身DNA，以及与损伤相关的分子模式（DAMP），例如从受损或受伤的细胞。此类DNA的传感分别通过干扰素调节因子3（IRF3）和核因子κB（NF-κB）的激活产生I型干扰素（IFN）和促炎性细胞因子来引发先天性免疫反应。这些细胞因子是固有免疫和适应性免疫反应相互联系的关键因素。但是，DNA传感器及其信号级联的缺陷会导致免疫反应失调，自身免疫性疾病，和癌症进展。在这里，我们提供了对病原体感染和细胞损伤的反应中DNA信号通路的更新，以及调节剂在控制免疫系统和维持宿主体内稳态方面的作用。我们还讨论了病原体对免疫监视的规避。