Abstract
Antiviral innate immunity works as the first line of host defense against viral infection. Pattern recognition receptors (PRRs) and adaptor proteins involved in the innate immune signaling pathways play critical roles in controlling viral infections via the induction of type I interferon and its downstream interferon-stimulated genes. Dynamic changes of adaptor proteins contribute to precise regulation of the activation and shut-off of signaling transduction, though numerous complex processes are involved in achieving dynamic changes to various proteins of the host and viruses. In this review, we will summarize recent progress on the trafficking patterns and conformational transitions of the adaptors that are involved in the antiviral innate immune signaling pathway during viral DNA sensing. Moreover, we aim to dissect the relationships between protein dynamics and DNA-sensing antiviral innate immune responses, which will reveal the underlying mechanisms controlling protein activity and maintaining cell homeostasis. By comprehensively revealing protein dynamics in cytosolic DNA-sensing antiviral innate immune signaling pathways, we will be able to identify potential new targets for the therapies of certain autoimmune diseases.
Highlights
Cellular processes are dependent on transmembrane receptors to communicate and transmit various signals into intracellular compartments
As the host’s frontline defense against viral infection, antiviral innate immunity is mainly triggered by the interaction between pattern recognition receptors (PRRs) and viral pathogen-associated molecular patterns (PAMPs), followed by the activation of downstream adaptor proteins, such as stimulator of interferon genes (STING), mitochondrial antiviral signaling protein (MAVS), tumor necrosis factor receptor-associated factor (TRAFs), Toll/IL-1 receptor domain-containing adaptor inducing IFN-β (TRIF), and some other adaptors, which contribute to the induction of type I interferons (IFN-I)
Evidence has shown that protein trafficking in innate immunity is critical to signaling transduction
Summary
Cellular processes are dependent on transmembrane receptors to communicate and transmit various signals into intracellular compartments. Dynamic changes in proteins precisely regulate the activation and inhibition of the signaling transduction. As the host’s frontline defense against viral infection, antiviral innate immunity is mainly triggered by the interaction between pattern recognition receptors (PRRs) and viral pathogen-associated molecular patterns (PAMPs), followed by the activation of downstream adaptor proteins, such as stimulator of interferon genes (STING), mitochondrial antiviral signaling protein (MAVS), tumor necrosis factor receptor-associated factor (TRAFs), Toll/IL-1 receptor domain-containing adaptor inducing IFN-β (TRIF), and some other adaptors, which contribute to the induction of type I interferons (IFN-I). In host antiviral innate immunity signaling pathways, protein trafficking is one of the primary protein dynamics essential for the activation of the signaling pathway. STING, the only receptor of cGAMP, moves from the endoplasmic reticulum
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