Innate immune RNA sensor

Innate immune RNA sensors are a specialized group of pattern recognition receptors (PRRs) responsible for detecting foreign or misplaced ribonucleic acids within the host cell (1.2.1, 1.2.2). These sensors are strategically localized in endosomes, such as Toll-like receptors (TLR) 3, 7, and 8, and the cytoplasm, including RIG-I-like receptors (RLRs) like RIG-I and MDA5, to monitor for viral genomes or replication intermediates (1.2.4, 1.4.1). Upon activation by specific RNA ligands, such as double-stranded RNA or 5-triphosphorylated RNA, these sensors initiate signaling pathways that culminate in the production of Type I interferons and pro-inflammatory cytokines (1.1.3, 1.2.5). This response is critical for establishing an antiviral state and bridging innate and adaptive immunity (1.4.3). In clinical settings, agonists of these sensors, such as Imiquimod and Poly(I:C), are utilized as vaccine adjuvants and in cancer immunotherapy to stimulate robust immune responses against pathogens or tumors (1.1.3, 1.2.4). Conversely, inappropriate activation of these sensors by endogenous RNA can lead to severe autoimmune and inflammatory diseases, such as systemic lupus erythematosus, making them important targets for inhibitory therapies (1.2.2, 1.2.4).

Other names

Host innate RNA sensorsRNA-sensing pattern recognition receptorsCytosolic RNA sensorsEndosomal RNA sensorsNucleic acid sensors

Activation of sensors (agonism) triggers the production of Type I interferons and pro-inflammatory cytokines via IRF3/7 and NF-kB pathways to enhance antiviral or antitumor immunity; inhibition (antagonism) prevents aberrant immune activation and chronic inflammation.