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Damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs) are diverse sets of molecules that serve as "danger signals" to initiate and perpetuate the innate immune response [1]. PAMPs are highly conserved molecular structures produced by microorganisms, such as lipopolysaccharides (LPS) from bacteria or viral double-stranded RNA, which are recognized as foreign by the host [2]. In contrast, DAMPs are endogenous molecules, such as High mobility group box 1 (HMGB1), S100 proteins, or extracellular ATP, that are released or exposed following cellular stress, injury, or non-programmed cell death [3]. Both classes of molecules exert their biological effects by binding to pattern recognition receptors (PRRs), including Toll-like receptors (TLRs) and NOD-like receptors (NLRs), triggering signaling cascades that lead to the production of pro-inflammatory cytokines and type I interferons [4]. In clinical contexts, the dysregulation or chronic presence of DAMPs and PAMPs is central to the pathogenesis of sepsis, autoimmune disorders, and chronic inflammatory diseases [2]. Therapeutic strategies often focus on neutralizing specific DAMPs/PAMPs or antagonizing their respective PRRs to mitigate excessive inflammation, though such interventions must balance the need for immune suppression with the risk of opportunistic infections [5].
Neutralization of circulating ligands or blockade of their cognate pattern recognition receptors (PRRs) to inhibit downstream pro-inflammatory signaling pathways.
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