Abstract
Innate immunity is the frontline of defense against infections and tissue damage. It is a fast and semi-specific response involving a myriad of processes essential for protecting the organism. These reactions promote the clearance of danger by activating, among others, an inflammatory response, the complement cascade and by recruiting the adaptive immunity. Any disequilibrium in this functional balance can lead to either inflammation-mediated tissue damage or defense inefficiency. A dynamic and coordinated gene expression program lies at the heart of the innate immune response. This expression program varies depending on the cell-type and the specific danger signal encountered by the cell and involves multiple layers of regulation. While these are achieved mainly via transcriptional control of gene expression, numerous post-transcriptional regulatory pathways involving RNA-binding proteins (RBPs) and other effectors play a critical role in its fine-tuning. Alternative splicing, translational control and mRNA stability have been shown to be tightly regulated during the innate immune response and participate in modulating gene expression in a global or gene specific manner. More recently, microRNAs assisting RBPs and post-transcriptional modification of RNA bases are also emerging as essential players of the innate immune process. In this review, we highlight the numerous roles played by specific RNA-binding effectors in mediating post-transcriptional control of gene expression to shape innate immunity.
Highlights
Host’s defense mechanisms form a complex interplay between molecular and cellular actors and require a plethora of processes to detect and eliminate pathogens or damage, such as loss of tissue integrity, irritants, or cancer
Inflammasome-forming nucleotide-binding domain leucine-rich repeat (NLR) proteins are a group of cytosolic Pattern Recognition Receptors (PRRs) that assemble inflammasome in response to Pathogen Associated Molecular Patterns (PAMPs) and DAMPs
Through their capacity to interact with specific RNA sequences, structural features or chemical modifications, RNA-binding proteins (RBPs) orchestrate all steps of RNA metabolism from its synthesis, maturation and functional role, to its eventual decay
Summary
Host’s defense mechanisms form a complex interplay between molecular and cellular actors and require a plethora of processes to detect and eliminate pathogens or damage, such as loss of tissue integrity, irritants, or cancer. Each family of PRRs recruits a specific adaptor such as myeloid differentiation primary response 88 (MyD88), mitochondrial antiviral signaling protein (MAVS) or stimulator of interferon genes (STING) for TLRs, RLRs or cGAS, respectively (Figure 1A). This initiates a signaling cascade, mostly involving IRF3/7, MAPK and NFkB pathways, leading to the expression of type I and III IFN [10, 11] and/or the secretion of cytokines, that orchestrate the various events happening during the inflammation process [12, 13], or chemokines, that will attract immune cells to the affected tissue. We review the multiple roles played by RBPs in shaping the innate immune response, from pathogen and danger detection to the regulation of signal transduction and effector functions
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