Abstract
Recognition of pathogen-derived nucleic acids by pattern-recognition receptors (PRRs) is essential for eliciting antiviral immune responses by inducing the production of type I interferons (IFNs) and proinflammatory cytokines. Such responses are a prerequisite for mounting innate and pathogen-specific adaptive immune responses. However, host cells also use nucleic acids as carriers of genetic information, and the aberrant recognition of self-nucleic acids by PRRs is associated with the onset of autoimmune or autoinflammatory diseases. In this review, we describe the mechanisms of nucleic acid sensing by PRRs, including Toll-like receptors, RIG-I-like receptors, and DNA sensor molecules, and their signaling pathways as well as the disorders caused by uncontrolled or unnecessary activation of these PRRs.
Highlights
The innate immune system is the first line of host defense against invading pathogens but is essential for the biological responses of the host against various harmful stimuli
The initiation of immune responses occurs via germline-encoded pattern-recognition receptors (PRRs), which recognize widely conserved features in pathogens, termed pathogen-associated molecular patterns (PAMPs), as well as “danger signals”, host components released in response to cell or tissue injury, termed damage-associated molecular patterns (DAMPs)
Because all pathogens possess nucleic acids, a defensive barrier network consisting of PRRs recognizing pathogenic DNA or RNA as PAMPs and their downstream signaling pathways is important for host protection against invading pathogens such as viruses and bacteria
Summary
INSERM UMR_S1110 Institute de Recherche sur les Maladies Virales et Hepatiques, France. Vanja Sisirak, UMR5164 Immunologie Conceptuelle, Experimentale et Translationnelle (Immuno ConcEpT), France. Signaling Through Nucleic Acid Sensors and Their Roles in Inflammatory Diseases. Recognition of pathogen-derived nucleic acids by pattern-recognition receptors (PRRs) is essential for eliciting antiviral immune responses by inducing the production of type I interferons (IFNs) and proinflammatory cytokines. Such responses are a prerequisite for mounting innate and pathogen-specific adaptive immune responses. We describe the mechanisms of nucleic acid sensing by PRRs, including Toll-like receptors, RIG-I-like receptors, and DNA sensor molecules, and their signaling pathways as well as the disorders caused by uncontrolled or unnecessary activation of these PRRs
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