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Gut-associated lymphoid tissue (GALT) immune cells represent the largest collection of lymphoid cells in the human body, distributed throughout the gastrointestinal tract in organized structures like Peyer's patches and isolated lymphoid follicles, as well as diffusely in the lamina propria [6, 7, 9]. This diverse population, including T cells, B cells, dendritic cells, and macrophages, is essential for maintaining mucosal homeostasis by balancing the induction of immune tolerance to dietary antigens and commensal microbiota with robust defense against enteric pathogens [2, 5, 10]. In pathological states such as inflammatory bowel disease (IBD), the dysregulated recruitment and activation of these cells drive chronic mucosal inflammation, while in HIV infection, GALT serves as a critical reservoir for viral replication and a site of early, profound CD4+ T cell depletion [1, 4, 14]. Therapeutic interventions often target GALT immune cells by inhibiting their gut-specific homing—primarily through the blockade of the alpha4beta7 integrin/MAdCAM-1 axis—or by utilizing GALT-targeted drug delivery systems to concentrate immunomodulators within the intestinal lymphatic environment [3, 4, 14].
Inhibition of lymphocyte trafficking to the gut mucosa by blocking integrin-mediated adhesion to MAdCAM-1, or direct modulation of local immune cell activity [4, 14].
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