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The Pattern recognition receptor (PRR) pathway is a critical system of the innate immune response that identifies conserved molecular motifs from pathogens (PAMPs) or damaged host cells (DAMPs) (Kawai & Akira, 2010). This pathway involves several distinct classes of receptors, including Toll-like receptors (TLRs), NOD-like receptors (NLRs), and RIG-I-like receptors (RLRs), which are located on the cell surface, in endosomes, or within the cytoplasm (Janeway & Medzhitov, 2002). Activation of these receptors initiates signaling cascades, often involving NF-κB or IRF transcription factors, resulting in the secretion of pro-inflammatory cytokines and interferons (Thompson et al., 2011). While essential for host defense against infections, aberrant PRR signaling is a major driver of chronic inflammation, autoimmune diseases, and metabolic disorders (Moresco et al., 2011). Pharmacological intervention typically targets specific receptors within the pathway; for instance, TLR7/8 agonists like imiquimod are used for skin cancers and viral warts, while TLR4 agonists serve as vaccine adjuvants (Kawai & Akira, 2011). Conversely, antagonists are being developed to mitigate the "cytokine storm" seen in severe infections or systemic lupus erythematosus (Li & Wu, 2021). Because the pathway involves multiple distinct receptor families, therapeutic targeting is usually specific to individual receptors rather than the entire pathway.
Drugs modulate the PRR pathway by acting as agonists to stimulate immune responses for vaccines and oncology, or as antagonists to inhibit overactive signaling in autoimmune and inflammatory diseases (Kawai & Akira, 2011; Li & Wu, 2021).
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