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Oral tolerance refers to the active immunological process in which oral exposure to an antigen—usually dietary proteins or administered therapeutic antigens—induces local and systemic hyporesponsiveness, primarily via expansion of regulatory T cells and other immune modulatory mechanisms[1][2][3][4]. This process is mediated by gut-associated lymphoid tissue, with key roles for dendritic cells, Tregs (Foxp3+ and Foxp3–), cytokines (e.g., IL-10, TGF-β), and the gut microbiota, allowing discrimination between harmful and harmless antigens encountered in the gastrointestinal tract. Oral tolerance underpins multiple immunotherapeutic strategies (such as antigen-specific oral immunotherapy for food allergies and autoimmune diseases) but is not itself a molecular target or receptor[1][2][4][6].
Induction of regulatory T cells (Tregs); Clonal deletion or anergy of effector T cells; Generation of antigen-specific immune hyporesponsiveness through repeated oral antigen exposure; Modulation of dendritic cell function, especially CD103+ DCs, in gut mucosa.
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