Oral tolerance can be defined as an inhibition of specific immune responsiveness to subsequent parenteral injections of proteins to which an individual or animal has been previously exposed via the oral route. Multiple mechanisms of tolerance are induced by oral-fed antigens, but induction of regulatory CD4 T-cells expressing the transcription factor Foxp3 and the membrane-bound TGF-β stands out as the major players in oral tolerance. Oral antigen administration suppresses several animal models of autoimmune disease, including experimental autoimmune encephalomyelitis, uveitis, thyroiditis, myasthenia, arthritis, and diabetes, but also nonautoimmune inflammatory conditions such as asthma, atherosclerosis, graft rejection, allergy, and stroke. However, human trials have produced mixed results, and a great deal remains to be learned about the mechanisms of oral tolerance before it can be successfully applied to people. In this review, we highlight the cellular components involved in oral tolerance induction. A deep knowledge of these intricate cell interactions will pave the way for a successful application of antigen tolerance to treat autoimmune and nonautoimmune inflammatory diseases.

中文翻译：

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口腔耐受诱导的细胞成分和机制。

口服耐受性可以定义为对随后的肠胃外注射蛋白质的特异性免疫应答的抑制作用，该蛋白质先前已经通过口服途径暴露于个体或动物。口服喂养的抗原诱导了多种耐受机制，但诱导表达转录因子Foxp3和膜结合的TGF-β的调节性CD4 T细胞是口服耐受的主要参与者。口服抗原可抑制多种自身免疫性疾病的动物模型，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，还可以抑制非自身免疫性炎症，例如哮喘，动脉粥样硬化，移植排斥，过敏和中风。但是，人体试验产生了不同的结果，在成功将口头耐受性应用到人们之前，还有很多关于口头耐受机制的知识需要学习。在这篇综述中，我们重点介绍了诱导口腔耐受的细胞成分。对这些复杂的细胞相互作用的深入了解将为成功应用抗原耐受性治疗自身免疫性和非自身免疫性炎性疾病铺平道路。