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Host immune pattern recognition and antimicrobial pathways represent the primary defense systems used by the innate immune system to identify and neutralize invading pathogens. These pathways are triggered by Pattern Recognition Receptors (PRRs), including Toll-like receptors (TLRs), NOD-like receptors (NLRs), and RIG-I-like receptors (RLRs), which detect conserved molecular signatures known as pathogen-associated molecular patterns (PAMPs) [1][2]. Activation of these receptors initiates complex intracellular signaling cascades that culminate in the production of pro-inflammatory cytokines, type I interferons, and antimicrobial peptides [3][4]. While essential for clearing infections, chronic or excessive activation of these pathways is a hallmark of various inflammatory and autoimmune diseases, such as rheumatoid arthritis and lupus [5]. Pharmacological intervention typically involves the use of PRR agonists as vaccine adjuvants or PRR antagonists to dampen pathological inflammation [6]. Because this term describes a broad collection of biological processes rather than a single molecular entity, it is classified as a pathway category rather than a specific therapeutic target.
Modulation of pattern recognition receptors (PRRs) or downstream signaling components to either stimulate innate immunity (agonism) or suppress pathological inflammation (antagonism).
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