Role of orally induced regulatory T cells in immunotherapy and tolerance.

Role of orally induced regulatory T cells in immunotherapy and tolerance.
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DOI:
10.1016/j.cellimm.2020.104251
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发表时间:
2021-01
影响因子:
4.3
通讯作者:
Piñeros AR
Piñeros AR
中科院分区:
医学4区
文献类型:
--
作者:
Bertolini TB;Biswas M;Terhorst C;Daniell H;Herzog RW;Piñeros AR

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口服抗原诱导调节性 T 细胞 (Treg) 利用胃肠道的调节机制来促进对食物抗原或共生微生物的无反应。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将树突状细胞 (DC) 调节为耐受性表型,通过表达多种介质(例如 Treg)诱导 Treg。 IL-10、转化生长因子-β、视黄酸。多种因素,例如源自微生物群或饮食的代谢物,影响这些诱导性 Treg 的稳定性和扩增,其中包括但不限于 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的作用的潜在机制。
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.
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