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Inflammatory peptides represent a broad and heterogeneous functional category of signaling molecules that play central roles in the initiation, amplification, and resolution of inflammatory responses [2, 8]. This group encompasses various sub-classes, including pro-inflammatory cytokines (e.g., tumor necrosis factor and interleukins), chemokines that regulate leukocyte recruitment, and neuropeptides such as substance P and calcitonin gene-related peptide (CGRP) that mediate neurogenic inflammation [10, 12]. These peptides typically function by binding to specific cell-surface receptors, such as G protein-coupled receptors (GPCRs) or cytokine receptors, thereby activating downstream signaling pathways like NF-κB and MAPK [5, 10]. Dysregulation of these peptide systems is a hallmark of numerous chronic conditions, including rheumatoid arthritis, inflammatory bowel disease, and migraine [2, 5]. Consequently, they are high-value targets in drug discovery, with therapeutic strategies focusing on neutralizing the peptide ligands with monoclonal antibodies or blocking their receptors with small molecules and biologics [1, 7]. While individual members of this class are specific therapeutic targets, the term inflammatory peptides itself refers to a functional grouping rather than a single molecular entity [8, 9].
Neutralization of pro-inflammatory peptide ligands or antagonism of their respective receptors to modulate the inflammatory cascade.
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