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Gut-associated immune cell receptors are a diverse group of surface proteins, including integrins (e.g., alpha-4/beta-7) and chemokine receptors (e.g., CCR9), that regulate the trafficking and activation of leukocytes within the gastrointestinal mucosa (Garside & Mowat, 2001, Nature Reviews Immunology). These receptors facilitate the selective recruitment of immune cells to the gut-associated lymphoid tissue (GALT) by interacting with tissue-specific ligands such as MAdCAM-1 and CCL25 (Eksteen et al., 2004, Journal of Experimental Medicine). In inflammatory bowel diseases (IBD), such as Crohn's disease and ulcerative colitis, the dysregulated expression and activation of these receptors lead to excessive leukocyte infiltration and chronic inflammation (Zundler et al., 2019, Gut). Therapeutic agents like vedolizumab, a monoclonal antibody targeting the alpha-4/beta-7 integrin, have been developed to specifically inhibit this gut-homing mechanism, providing a targeted approach to treating IBD with reduced systemic side effects (Feagan et al., 2013, New England Journal of Medicine). Other targets within this category include CCR9 and various Toll-like receptors (TLRs) that modulate innate immune responses to the gut microbiota (Kaser et al., 2010, Annual Review of Immunology). By blocking these receptors, drugs can effectively reduce the local inflammatory burden without compromising the broader immune system's ability to fight systemic infections.
Antagonism of cell surface receptors (e.g., alpha-4/beta-7 integrin, CCR9) to inhibit the recruitment of pro-inflammatory leukocytes to the gastrointestinal tract or modulation of innate immune signaling pathways.
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