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Innate immune receptors and structural cells refers to the collective system of pattern recognition receptors (PRRs) expressed by non-hematopoietic cells, such as epithelial cells, fibroblasts, and endothelial cells (Krausgruber et al., 2020, Nature) [1]. These structural cells function as active immune sentinels, utilizing receptors like Toll-like receptors (TLRs), NOD-like receptors (NLRs), and RIG-I-like receptors (RLRs) to detect pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) (Whitsett and Alenghat, 2015, Nature) [2]. Upon activation, these cells initiate inflammatory signaling cascades, producing cytokines, chemokines, and antimicrobial peptides that shape the local immune environment (Hammad and Lambrecht, 2008, Nature Reviews Immunology) [3]. Dysregulation of these pathways in structural cells is a key driver of chronic inflammatory conditions, including asthma, chronic obstructive pulmonary disease (COPD), and inflammatory bowel disease (IBD) (Iwasaki and Medzhitov, 2015, Science) [4]. While specific receptors within this category, such as TLR7 or NLRP3, are major therapeutic targets, the term itself describes a broad biological interface rather than a single druggable molecule (Takeuchi and Akira, 2010, Cell) [5]. Consequently, therapeutic strategies focus on modulating specific PRRs to either enhance host defense or dampen pathological inflammation in a tissue-specific manner (Kawai and Akira, 2011, Nature Immunology) [6].
Modulation of pattern recognition receptors (PRRs) expressed on structural cells to regulate the production of pro-inflammatory cytokines, chemokines, and antimicrobial peptides.
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