Oral tolerance (OT) has classically been defined as the specific suppression of cellular and/or humoral immune responses to an antigen by prior administration of the antigen through the oral route. Multiple mechanisms have been proposed to explain the induction of OT including T cell clonal depletion and anergy when high doses of antigens are fed, and regulatory T (Treg) cell generation following oral administration of low and repeated doses of antigens. Oral antigen administration suppresses the immune response in several animal models of autoimmune disease, including experimental autoimmune encephalomyelitis, uveitis, thyroiditis, myasthenia, arthritis and diabetes, but also non-autoimmune inflammatory conditions such as asthma, atherosclerosis, graft rejection, allergy and stroke. However, human trials have given mixed results and a great deal remains to be learned about the mechanisms of OT before it can be successfully applied to people. One of the possible mechanisms relates to the gut microbiota and in this review, we will explore the cellular components involved in the induction of OT and the role of the gut microbiota in contributing to OT development.

口服耐受 (OT) 经典地定义为通过预先通过口服途径施用抗原来特异性抑制对抗原的细胞和/或体液免疫应答。已经提出了多种机制来解释 OT 的诱导，包括喂食高剂量抗原时的 T 细胞克隆耗竭和无反应性，以及口服低剂量和重复剂量的抗原后调节性 T (Treg) 细胞的产生。口服抗原可抑制多种自身免疫性疾病动物模型的免疫反应，包括实验性自身免疫性脑脊髓炎、葡萄膜炎、甲状腺炎、肌无力、关节炎和糖尿病，以及非自身免疫性炎症，如哮喘、动脉粥样硬化、移植排斥、过敏和中风。然而，人体试验的结果喜忧参半，在成功应用于人体之前，关于 OT 的机制还有很多需要了解。其中一种可能的机制与肠道微生物群有关，在本综述中，我们将探讨参与诱导 OT 的细胞成分以及肠道微生物群在促进 OT 发育中的作用。