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Innate pattern recognition receptors (PRRs) are a diverse group of germline-encoded proteins that serve as the primary sensors of the innate immune system, detecting pathogen-associated molecular patterns (PAMPs) (Janeway & Medzhitov, 2002). In the context of viral infections, these receptors identify virion-associated components such as double-stranded RNA (dsRNA), single-stranded RNA (ssRNA), and cytosolic DNA (Kawai & Akira, 2010). Key families involved in sensing viral PAMPs include Toll-like receptors (TLRs 3, 7, 8, and 9), RIG-I-like receptors (RLRs such as RIG-I and MDA5), and cytosolic DNA sensors like cGAS (Thompson et al., 2011). Upon activation, these receptors trigger signaling pathways involving adaptor proteins like MyD88, TRIF, MAVS, or STING, leading to the production of type I interferons (IFNs) and pro-inflammatory cytokines (Wu & Chen, 2014). This response is critical for establishing an antiviral state and bridging innate and adaptive immunity (Iwasaki & Medzhitov, 2015). Therapeutically, PRR agonists are utilized as vaccine adjuvants and in cancer immunotherapy to stimulate robust immune responses (Steinhagen et al., 2011). Conversely, PRR signaling is often dysregulated in chronic inflammatory and autoimmune diseases, making these pathways targets for inhibitory strategies (Roers et al., 2016). The development of drugs targeting these receptors requires careful balancing of immune activation to avoid systemic toxicity or autoimmunity (Dubyak, 2016).
Agonism of specific PRRs (e.g., TLR7, TLR9, RIG-I) to induce type I interferon and pro-inflammatory cytokine production for antiviral or antitumor activity; Antagonism to suppress pathological inflammation.
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