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Toll-like receptors (TLRs) on intestinal epithelial cells (IECs) are membrane-bound pattern recognition receptors critical for sensing microbial components and danger signals in the gut. They are expressed at lower levels than in immune cells and demonstrate polarized localization within IECs (apical, basolateral, or intracellular compartments, depending on TLR and cell type)[2][3][5]. TLR signaling orchestrates immune responses, regulates antimicrobial peptide production, and maintains epithelial barrier integrity, balancing defense against pathogens with avoidance of excessive inflammation to commensal microbes[1][2][4][5]. Dysregulation of TLRs on IECs has been implicated in the pathogenesis of inflammatory bowel diseases, colorectal cancer, and alterations in gut microbiota homeostasis[1][4][5]. TLRs act both as sensors and mediators in the gut, directing appropriate host immune responses and influencing disease outcomes through control of cytokine production and barrier function[4][5].
Agonism or antagonism of TLRs to modulate downstream inflammatory pathways (such as NF-κB activation); Modulation of cytokine and chemokine production
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