Oral antigen administration to induce regulatory T cells (Treg) takes advantage of regulatory mechanisms that the gastrointestinal tract utilizes to promote unresponsiveness against food antigens or commensal microorganisms. Recently, antigen-based oral immunotherapies (OITs) have shown efficacy as treatment for food allergy and autoimmune diseases. Similarly, OITs appear to prevent anti-drug antibody responses in replacement therapy for genetic diseases. Intestinal epithelial cells and microbiota possibly condition dendritic cells (DC) toward a tolerogenic phenotype that induces Treg via expression of several mediators, e.g. IL-10, transforming growth factor-β, retinoic acid. Several factors, such as metabolites derived from microbiota or diet, impact the stability and expansion of these induced Treg, which include, but are not limited to, FoxP3⁺ Treg, LAP⁺ Treg, and/or Tr1 cells. Here, we review various orally induced Treg, their plasticity and cooperation between the Treg subsets, as well as underlying mechanisms controlling their induction and role in oral tolerance.

用于诱导调节性 T 细胞 (Treg) 的口服抗原给药利用了胃肠道用来促进对食物抗原或共生微生物无反应的调节机制。最近，基于抗原的口服免疫疗法 (OIT) 已显示出治疗食物过敏和自身免疫性疾病的功效。同样，OIT 似乎可以防止遗传疾病替代疗法中的抗药物抗体反应。肠上皮细胞和微生物群可能使树突状细胞 (DC) 趋向耐受性表型，该表型通过几种介质的表达诱导 Treg，例如IL-10、转化生长因子-β、视黄酸。一些因素，例如来自微生物群或饮食的代谢物，会影响这些诱导的 Treg 的稳定性和扩增，包括但不限于 FoxP3 ⁺ Treg、LAP ⁺ Treg 和/或 Tr1 细胞。在这里，我们回顾了各种口服诱导的 Treg、它们的可塑性和 Treg 亚群之间的合作，以及控制它们的诱导和在口服耐受中作用的潜在机制。