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Innate immune system sensors, most commonly referred to as **pattern recognition receptors (PRRs)**, are a diverse group of germline-encoded receptor proteins that detect conserved molecular patterns found in pathogens (PAMPs) and endogenous danger signals (DAMPs)[2][5]. Major classes of these receptors include **Toll-like receptors (TLRs)**, **NOD-like receptors (NLRs)**, **C-type lectin receptors (CLRs)**, **AIM2-like receptors (ALRs)**, **cyclic GMP-AMP synthase (cGAS)**, and **RIG-I-like receptors (RLRs)** such as RIG-I and MDA-5[2][5][3]. Upon activation, these sensors initiate signaling cascades (e.g., via the STING, MAVS, or inflammasome pathways) that lead to rapid induction of type I interferons and other cytokines, development of inflammation, and stimuli for adaptive immune responses[1][3][4][6]. Dysregulation or improper targeting of these pathways can contribute to inflammatory diseases, autoimmunity, or cancer progression[7]. Currently, “innate immune system sensors and pathways” is not a specific molecular target but rather refers to an entire class of innate immune receptors and their associated signaling networks[2][4]; for structured database purposes, these should be mapped to the specific receptor or molecular pathway of interest (e.g., "Toll-like receptor 4" instead of the broad category).
Agonism or antagonism of signal initiation through PRRs (such as Toll-like receptor agonists/antagonists); Inhibition or activation of downstream signaling pathways leading to interferon or cytokine production.
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