Host innate immune receptors and epithelial cells

This entry refers to the complex interface between host pattern recognition receptors (PRRs) and the epithelial cells that form the primary barrier against environmental insults. Epithelial cells in the respiratory, gastrointestinal, and urogenital tracts express a diverse array of PRRs, including Toll-like receptors (TLRs), NOD-like receptors (NLRs), and RIG-I-like receptors (RLRs), which allow them to sense pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) [Schleimer et al., 2007, Nature Reviews Immunology]. Upon activation, these receptors trigger intracellular signaling cascades, such as the NF-κB and IRF pathways, leading to the production of pro-inflammatory cytokines, chemokines, and antimicrobial peptides [Akira et al., 2006, Cell]. This process effectively initiates the host's innate immune response and coordinates the transition to adaptive immunity [Artis, 2008, Nature]. Dysregulation of this interaction is central to the pathogenesis of various inflammatory and infectious diseases, such as asthma, inflammatory bowel disease (IBD), and viral pneumonia [Vareille et al., 2011, Clinical Microbiology Reviews]. While not a single therapeutic target, specific components within this system, such as TLR4 or NLRP3, are major focuses of drug development for modulating inflammation and enhancing vaccine efficacy [Kawai & Akira, 2011, Nature Immunology]. Drugs like Imiquimod and Monophosphoryl lipid A target these receptors to stimulate immune responses, while various antagonists are being explored to treat chronic inflammatory conditions [Moresco et al., 2011, Nature Immunology].

Other names

Epithelial innate immune systemMucosal pattern recognition receptorsEpithelial-immune interfaceEpithelial PRRs

Modulation of pattern recognition receptor signaling to regulate the production of inflammatory mediators and maintain epithelial barrier homeostasis.