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Intestinal innate and adaptive immune receptors represent a broad category of proteins responsible for sensing the luminal environment and coordinating immune responses within the gastrointestinal tract (Mowat & Agace, 2014). Innate receptors, such as Toll-like receptors (TLRs) and NOD-like receptors (NLRs), act as the first line of defense by recognizing pathogen-associated molecular patterns (PAMPs) from bacteria, viruses, and fungi (Abraham & Medzhitov, 2011). Adaptive receptors, including T-cell receptors (TCRs) and B-cell receptors (BCRs), facilitate highly specific responses to antigens and are crucial for maintaining long-term mucosal immunity and tolerance to commensal microbes (Round & Mazmanian, 2009). The balance between these systems is vital for gut health; however, their overactivation or dysfunction is central to the pathogenesis of chronic inflammatory diseases like Crohn's disease and ulcerative colitis (Danese & Fiocchi, 2011). Therapeutic strategies often target these pathways by inhibiting specific receptors, such as integrins or sphingosine-1-phosphate receptors, or by blocking the signaling cascades initiated by these receptors (Neurath, 2014). Understanding the interplay between these innate and adaptive components is essential for developing targeted biologics and small molecules that can restore intestinal health.
Modulation of mucosal immune signaling, inhibition of leukocyte trafficking to the gut (e.g., via α4β7 integrin blockade), and neutralization of pro-inflammatory cytokine pathways (Neurath, 2014).
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