Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.
Proc Natl Acad Sci U S A. 2012 Jul 10;109(28):11270-5. doi: 10.1073/pnas.1120611109. Epub 2012 Jun 27.
The immune response is normally controlled by regulatory T cells (Tregs). However, Treg deficits are found in autoimmune diseases, and therefore the induction of functional Tregs is considered a potential therapeutic approach for autoimmune disorders. The activation of the ligand-activated transcription factor aryl hydrocarbon receptor by 2-(1'H-indole-3'-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) or other ligands induces dendritic cells (DCs) that promote FoxP3(+) Treg differentiation. Here we report the use of nanoparticles (NPs) to coadminister ITE and a T-cell epitope from myelin oligodendrocyte glycoprotein (MOG)(35)(-55) to promote the generation of Tregs by DCs. NP-treated DCs displayed a tolerogenic phenotype and promoted the differentiation of Tregs in vitro. Moreover, NPs carrying ITE and MOG(35-55) expanded the FoxP3(+) Treg compartment and suppressed the development of experimental autoimmune encephalomyelitis, an experimental model of multiple sclerosis. Thus, NPs are potential new tools to induce functional Tregs in autoimmune disorders.
免疫反应通常受调节性 T 细胞 (Treg) 控制。然而,在自身免疫性疾病中发现 Treg 缺陷,因此诱导功能性 Treg 被认为是治疗自身免疫性疾病的一种潜在方法。2-(1'H-吲哚-3'-羰基)-噻唑-4-羧酸甲酯 (ITE) 或其他配体激活配体激活转录因子芳香烃受体,诱导树突状细胞 (DC),促进 FoxP3(+)Treg 分化。本文报道了使用纳米颗粒 (NPs) 共给药 ITE 和髓鞘少突胶质糖蛋白 (MOG)(35)(-55) 的 T 细胞表位,以促进 DC 产生 Treg。NP 处理的 DC 表现出耐受性表型,并在体外促进 Treg 的分化。此外,携带 ITE 和 MOG(35-55)的 NPs 扩增了 FoxP3(+)Treg 区室,并抑制了实验性自身免疫性脑脊髓炎的发展,这是多发性硬化症的一种实验模型。因此,NP 是诱导自身免疫性疾病中功能性 Treg 的潜在新工具。