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Innate RNA-sensing pattern recognition receptors (PRRs) are a specialized class of immune sensors that detect non-self RNA molecules, typically associated with viral replication or cellular damage (Kawai & Akira, 2010). This group primarily comprises the endosomal Toll-like receptors (TLR3, TLR7, and TLR8) and the cytosolic RIG-I-like receptors (RIG-I and MDA5) (Loo & Gale, 2011). When these receptors encounter specific RNA ligands, such as double-stranded RNA or 5'-triphosphate RNA, they initiate signaling pathways through adapter proteins like TRIF or MAVS (Wu & Chen, 2014). This activation results in the robust production of type I interferons and pro-inflammatory cytokines, which are essential for establishing an antiviral state and modulating the adaptive immune response (Kawai & Akira, 2010). Dysregulation of these sensors is implicated in various pathologies; overactivation can lead to autoimmune interferonopathies like systemic lupus erythematosus, while insufficient activation may result in increased susceptibility to viral infections (Crow, 2011). Consequently, these receptors are major therapeutic targets, with agonists being utilized as vaccine adjuvants and cancer immunotherapies, and antagonists being investigated for the treatment of chronic inflammatory and autoimmune diseases (Wu & Chen, 2014).
Agonism of endosomal or cytosolic sensors to induce interferon production; Antagonism to suppress autoimmune signaling.
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