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Innate immune pattern-recognition receptors (PRRs) are a diverse class of germline-encoded sensors primarily expressed on antigen-presenting cells (APCs) such as dendritic cells and macrophages (Janeway and Medzhitov, 2002, Annu Rev Immunol). These receptors are specialized to detect pathogen-associated molecular patterns (PAMPs) from microbes and damage-associated molecular patterns (DAMPs) from host cells (Iwasaki and Medzhitov, 2015, Nat Immunol). Major families include Toll-like receptors (TLRs), NOD-like receptors (NLRs), RIG-I-like receptors (RLRs), and the cGAS-STING pathway (Thompson et al., 2011, Viruses). Activation of these pathways triggers signaling cascades that lead to the production of pro-inflammatory cytokines and type I interferons, which are essential for bridging innate and adaptive immunity (Kawai and Akira, 2010, Nat Immunol). In therapeutic contexts, PRR agonists like imiquimod and monophosphoryl lipid A are used as vaccine adjuvants or cancer immunotherapies to stimulate robust T-cell responses (Kaczanowska et al., 2013, Front Immunol). Conversely, the overactivation or dysregulation of these pathways is implicated in chronic inflammatory and autoimmune diseases, making them targets for inhibitory therapies (O'Neill et al., 2013, Nat Rev Immunol).
Agonism of specific receptors (e.g., TLRs, STING) to enhance immune activation or antagonism to suppress pathological inflammation (Kaczanowska et al., 2013, Front Immunol; O'Neill et al., 2013, Nat Rev Immunol).
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