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Innate immune pattern recognition pathways represent the fundamental sensing systems of the immune system, responsible for detecting conserved molecular signatures of microbes and host distress (Takeuchi & Akira, 2010, Cell). These pathways are mediated by various classes of Pattern Recognition Receptors (PRRs), including Toll-like receptors (TLRs), NOD-like receptors (NLRs), RIG-I-like receptors (RLRs), and C-type lectin receptors (CLRs) (Janeway & Medzhitov, 2002, Annu Rev Immunol). When these receptors encounter pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), they initiate intracellular signaling cascades involving adapters like MyD88 or TRIF (O'Neill et al., 2013, Nat Rev Immunol). This leads to the activation of transcription factors such as NF-κB and IRFs, resulting in the secretion of pro-inflammatory cytokines and type I interferons (Kawai & Akira, 2010, Nat Immunol). While essential for host defense, chronic or inappropriate activation of these pathways contributes to the pathogenesis of autoimmune diseases, metabolic disorders, and cancer (Kopp & Medzhitov, 2003, Curr Opin Immunol). Consequently, these pathways are major targets for drug development, with agonists like Imiquimod used as cancer immunotherapies and antagonists like NLRP3 inhibitors explored for treating chronic inflammatory conditions (Moresco et al., 2011, Nat Immunol).
Agonism or antagonism of specific pattern recognition receptors to modulate innate immune signaling and cytokine production.
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