Abstract
Pathogens can produce conserved pathogen-associated molecular patterns (PAMPs) after invading the body, which can be specifically recognized by host pattern recognition receptors (PRRs). In recent years, it has been found that cytoplasmic DNA receptors recognize exogenous DNA inducing activation of interferon 1 (IFN1), which is a rapid advance in various research areas. The cyclic GMP–AMP synthase (cGAS) stimulator of interferon gene (STING) signaling pathway is a critical natural immune pathway in cells. Early studies revealed that it plays a crucial regulatory role in pathogen infection and tumor, and it is associated with various human autoimmune diseases. Recently studies have found that activation of cGAS-STING signaling pathway is related to different organ injuries. The present review elaborates on the regulation of the cGAS-STING signaling pathway and its role in various diseases, aiming to provide a theoretical basis for immunotherapy targeting this pathway.
Highlights
As the most vital human defense system, the immune system exerts strength in safeguarding the body against damage from three aspects—immune defense, immune surveillance, and immune homeostasis
We mainly focus on reviewing the functional roles of the cyclic GMP–AMP synthase (cGAS)-stimulator of interferon gene (STING) pathway in diseases and different organ injuries
CGAS-STING activation increases type Ι IFNs through interferon regulatory transcription factor 3 (IRF3) and pro-inflammatory responses mediated by nuclear factor (NF)-κB (Barber, 2015), type 1 IFNs released by non-parenchymal cells (NPCs) are the main cause of radiation-induced liver damage (RILD) in liver cells
Summary
As the most vital human defense system, the immune system exerts strength in safeguarding the body against damage from three aspects—immune defense, immune surveillance, and immune homeostasis. The presence of BECN1 protein can increase autophagy-mediated cytoplasmic DNA degradation by inhibiting cGAS-STING signaling pathway (Ishikawa and Barber, 2008). DsDNA within broncho-alveolar space, caused by different mechanisms (damaged cells, defective repair of DNA damage, or ROS), promotes NETs formation and can be sensed by cGAS but not TLR9, inducing type I IFNs expression (Figure 3).
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