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首页> 外文期刊>AIDS Research and Human Retroviruses >Lentivirus-activated T regulatory cells suppress T helper cell interleukin-2 production by inhibiting nuclear factor of activated T cells 2 binding to the interleukin-2 promoter
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Lentivirus-activated T regulatory cells suppress T helper cell interleukin-2 production by inhibiting nuclear factor of activated T cells 2 binding to the interleukin-2 promoter

机译：慢病毒激活的T调节细胞通过抑制与白介素2启动子结合的活化T细胞2的核因子来抑制T辅助细胞白介素2的产生。

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Using the feline immunodeficiency virus (FIV) model for AIDS lentivirus infection, we previously demonstrated that Treg cells from FIV-infected cats up-regulate membrane-associated tumor growth factor beta (mTGF-?) during the course of infection and that activated T lymphocytes up-regulate TGF-? receptor II (TGF-?RII) during the course of infection. Furthermore, we have demonstrated that autologous coculture of Tregs with Th cells from FIV-infected cats leads to suppression of interleukin (IL)-2 production and loss of proliferation in a TGF-?-dependent fashion. Nuclear factor of activated T cells (NFAT) 2 has been identified as integral to effector Th cell maturation and function by promoting IL-2 transcription. Therefore, we questioned whether NFAT2 expression might be altered by TGF-β signaling. Feline NFAT2 exon sequences were identified based upon sequence homology to human and murine NFAT2. Following stimulation, IL-2 and NFAT2 mRNA levels were similarly increased in both FIV- and FIV+ cats. Activated CD4+CD25- cells from both FIV- and FIV + cats cocultured with autologous CD4+CD25+ cells or treated with TGF-β demonstrated decreased IL-2 production; however, NFAT2 mRNA levels were unaffected. Although NFAT2 mRNA levels were unaffected, chromatin immunoprecipitation (ChIP) for NFAT2 indicated decreased NFAT2 binding at the IL-2 promoter in suppressed Th cells. These data suggest that TGF-β-mediated Treg cell suppression of IL-2 transcription is modulated through alterations in NFAT2 binding to the IL-2 promoter.
机译：使用针对艾滋病毒慢病毒感染的猫免疫缺陷病毒（FIV）模型，我们以前证明了感染FIV的猫的Treg细胞在感染过程中上调了膜相关的肿瘤生长因子β（mTGF-β），并激活了T淋巴细胞上调TGF-？感染过程中的受体II（TGF-βRII）。此外，我们已经证明，Tregs与来自FIV感染的猫的Th细胞的自体共培养导致抑制白介素（IL）-2的产生和以TGF-β依赖性的方式丧失增殖。激活的T细胞（NFAT）2的核因子已被鉴定为效应Th细胞成熟和通过促进IL-2转录发挥功能所必需。因此，我们质疑TGF-β信号传导是否会改变NFAT2的表达。基于与人和鼠NFAT2的序列同源性，鉴定出猫NFAT2外显子序列。刺激后，FIV-和FIV +猫的IL-2和NFAT2 mRNA水平同样升高。与自体CD4 + CD25 +细胞共培养或经TGF-β处理的FIV-和FIV +猫的活化CD4 + CD25-细胞均显示IL-2产生减少。但是，NFAT2 mRNA水平不受影响。尽管NFAT2 mRNA水平不受影响，但NFAT2的染色质免疫沉淀（ChIP）表明抑制的Th细胞中IL-2启动子处的NFAT2结合减少。这些数据表明，TGF-β介导的Treg细胞对IL-2转录的抑制是通过改变与IL-2启动子结合的NFAT2来调节的。

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