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低剂量霍乱毒素及其介质环磷酸腺苷(cAMP)可诱导树突状细胞分泌CTLA-2,以增强调节性T细胞的转化。

Low doses of cholera toxin and its mediator cAMP induce CTLA-2 secretion by dendritic cells to enhance regulatory T cell conversion.

作者信息

Silva-Vilches Cinthia, Pletinckx Katrien, Lohnert Miriam, Pavlovic Vladimir, Ashour Diyaaeldin, John Vini, Vendelova Emilia, Kneitz Susanne, Zhou Jie, Chen Rena, Reinheckel Thomas, Mueller Thomas D, Bodem Jochen, Lutz Manfred B

机构信息

Institute of Virology and Immunobiology, University of Wuerzburg, Wuerzburg, Germany.

Department of Physiological Chemistry, University of Wuerzburg, Wuerzburg, Germany.

出版信息

PLoS One. 2017 Jul 31;12(7):e0178114. doi: 10.1371/journal.pone.0178114. eCollection 2017.

Abstract

Immature or semi-mature dendritic cells (DCs) represent tolerogenic maturation stages that can convert naive T cells into Foxp3+ induced regulatory T cells (iTreg). Here we found that murine bone marrow-derived DCs (BM-DCs) treated with cholera toxin (CT) matured by up-regulating MHC-II and costimulatory molecules using either high or low doses of CT (CThi, CTlo) or with cAMP, a known mediator CT signals. However, all three conditions also induced mRNA of both isoforms of the tolerogenic molecule cytotoxic T lymphocyte antigen 2 (CTLA-2α and CTLA-2β). Only DCs matured under CThi conditions secreted IL-1β, IL-6 and IL-23 leading to the instruction of Th17 cell polarization. In contrast, CTlo- or cAMP-DCs resembled semi-mature DCs and enhanced TGF-β-dependent Foxp3+ iTreg conversion. iTreg conversion could be reduced using siRNA blocking of CTLA-2 and reversely, addition of recombinant CTLA-2α increased iTreg conversion in vitro. Injection of CTlo- or cAMP-DCs exerted MOG peptide-specific protective effects in experimental autoimmune encephalomyelitis (EAE) by inducing Foxp3+ Tregs and reducing Th17 responses. Together, we identified CTLA-2 production by DCs as a novel tolerogenic mediator of TGF-β-mediated iTreg induction in vitro and in vivo. The CT-induced and cAMP-mediated up-regulation of CTLA-2 also may point to a novel immune evasion mechanism of Vibrio cholerae.

摘要

未成熟或半成熟的树突状细胞(DCs)代表了致耐受性成熟阶段,可将初始T细胞转化为Foxp3 +诱导调节性T细胞(iTreg)。在此,我们发现用霍乱毒素(CT)处理的小鼠骨髓来源的DCs(BM-DCs),通过使用高剂量或低剂量的CT(CThi、CTlo)或用环磷酸腺苷(cAMP,一种已知的CT信号介导物)上调MHC-II和共刺激分子而成熟。然而,所有这三种情况也诱导了耐受性分子细胞毒性T淋巴细胞抗原2的两种异构体(CTLA-2α和CTLA-2β)的mRNA表达。只有在CThi条件下成熟的DCs分泌IL-1β、IL-6和IL-23,从而导致Th17细胞极化的指令。相比之下,CTlo-或cAMP-DCs类似于半成熟DCs,并增强了TGF-β依赖的Foxp3 + iTreg转化。使用CTLA-2的siRNA阻断可降低iTreg转化,相反,添加重组CTLA-2α可在体外增加iTreg转化。注射CTlo-或cAMP-DCs通过诱导Foxp3 + Tregs并减少Th17反应,在实验性自身免疫性脑脊髓炎(EAE)中发挥对髓鞘少突胶质细胞糖蛋白(MOG)肽特异性的保护作用。总之,我们确定DCs产生的CTLA-2是体外和体内TGF-β介导的iTreg诱导的一种新型致耐受性介质。CT诱导和cAMP介导的CTLA-2上调也可能指向霍乱弧菌一种新的免疫逃避机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5047/5536293/4f7a6aaf0cd9/pone.0178114.g001.jpg

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