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【文摘发布】哺乳动物雷帕霉素靶蛋白在调节T细胞活化与无能中的作用

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这个帖子发布于13年零268天前,其中的信息可能已发生改变或有所发展。
Title:A role for mammalian target of rapamycin in regulating T cell activation versus anergy.

Author:Zheng Y, Collins SL, Lutz MA, Allen AN, Kole TP, Zarek PE, Powell JD.

source:J Immunol. 2007 Feb 15;178(4):2163-70.

IF:6.387(2005)

Whether TCR engagement leads to activation or tolerance is determined by the concomitant delivery of multiple accessory signals, cytokines, and environmental cues. In this study, we demonstrate that the mammalian target of rapamycin (mTOR) integrates these signals and determines the outcome of TCR engagement with regard to activation or anergy. In vitro, Ag recognition in the setting of mTOR activation leads to full immune responses, whereas recognition in the setting of mTOR inhibition results in anergy. Full T cell activation is associated with an increase in the phosphorylation of the downstream mTOR target S6 kinase 1 at Thr(421)/Ser(424) and an increase in the mTOR-dependent cell surface expression of transferrin receptor (CD71). Alternatively, the induction of anergy results in markedly less S6 kinase 1 Thr(421)/Ser(424) phosphorylation and CD71 surface expression. Likewise, the reversal of anergy is associated not with proliferation, but rather the specific activation of mTOR. Importantly, T cells engineered to express a rapamycin-resistant mTOR construct are resistant to anergy induction caused by rapamycin. In vivo, mTOR inhibition promotes T cell anergy under conditions that would normally induce priming. Furthermore, by examining CD71 surface expression, we are able to distinguish and differentially isolate anergic and activated T cells in vivo. Overall, our data suggest that by integrating environmental cues, mTOR plays a central role in determining the outcome of Ag recognition.
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2007-06-08 15:57 浏览 : 1097 回复 : 1
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xupeipei 编辑于 2007-06-18 23:56
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自己顶自己啰!

Title:A role for mammalian target of rapamycin in regulating T cell activation versus anergy.
题目: 哺乳动物雷帕霉素靶蛋白在调节T细胞活化与无能的作用
Author:Zheng Y, Collins SL, Lutz MA, Allen AN, Kole TP, Zarek PE, Powell JD.
作者: Zheng Y, Collins SL, Lutz MA, Allen AN, Kole TP, Zarek PE, Powell JD.
source:J Immunol. 2007 Feb 15;178(4):2163-70.
来源:免疫学杂志. 2007 2月 15;178(4):2163-70.
IF:6.387(2005)
影响因子: 6.387(2005)
Whether TCR engagement leads to activation or tolerance is determined by the concomitant delivery of multiple accessory signals, cytokines, and environmental cues.
TCR(T细胞受体)识别后产生激活或是耐受是由多种辅助信号,细胞因子和环境因素共同信号传递决定.
In this study, we demonstrate that the mammalian target of rapamycin (mTOR) integrates these signals and determines the outcome of TCR engagement with regard to activation or anergy.
本研究中,我们证实哺乳动物雷帕霉素靶蛋白(mTOR)整合这些信号并决定TCR识别后是产生激活或无能.
In vitro, Ag recognition in the setting of mTOR activation leads to full immune responses, whereas recognition in the setting of mTOR inhibition results in anergy.
体外研究中,在mTOR活化情况下识别抗原后将产生全免疫应答,而在mTOR抑制情况下则产生无能.
Full T cell activation is associated with an increase in the phosphorylation of the downstream mTOR target S6 kinase 1 at Thr(421)/Ser(424) and an increase in the mTOR-dependent cell surface expression of transferrin receptor (CD71).
全T细胞激活伴有下游mTOR标靶S6激酶1在421位苏氨酸/424位丝氨酸磷酸化的增加以及mTOR依赖性胞膜型转铁蛋白受体(CD71)的增加.
Alternatively, the induction of anergy results in markedly less S6 kinase 1 Thr(421)/Ser(424) phosphorylation and CD71 surface expression.
换之,无能可导致明显地S6激酶1在421位苏氨酸/424位丝氨酸磷酸化和CD71胞膜表达的减少.
Likewise, the reversal of anergy is associated not with proliferation, but rather the specific activation of mTOR.
相似地,逆转无能和增生无关,而与特异性mTOR活化相关.
Importantly, T cells engineered to express a rapamycin-resistant mTOR construct are resistant to anergy induction caused by rapamycin.
重要地是,T细胞表达人为构造的耐受雷帕霉素mTOR可对抗雷帕霉素诱导的无能.
In vivo, mTOR inhibition promotes T cell anergy under conditions that would normally induce priming.
体内研究中,在正常可激发免疫反应的条件下,抑制mTOR可促使T细胞无能.
Furthermore, by examining CD71 surface expression, we are able to distinguish and differentially isolate anergic and activated T cells in vivo.
另外,通过检测CD71的胞膜表达,我们能够在体内鉴别并分离无能与活化的T细胞.
Overall, our data suggest that by integrating environmental cues, mTOR plays a central role in determining the outcome of Ag recognition.
总之,我们的数据提示:通过整合各种环境因素, mTOR在决定抗原识别后的结果起重要作用.

(453字)
题目: 哺乳动物雷帕霉素靶蛋白在调节T细胞活化与无能的作用
作者: Zheng Y, Collins SL, Lutz MA, Allen AN, Kole TP, Zarek PE, Powell JD.
来源:免疫学杂志. 2007 2月 15;178(4):2163-70.
影响因子: 6.387(2005)

TCR(T细胞受体)识别后产生激活或是耐受是由多种辅助信号,细胞因子和环境因素共同信号传递决定.本研究中,我们证实哺乳动物雷帕霉素靶蛋白(mTOR)整合这些信号并决定TCR识别后是产生激活或无能.体外研究中,在mTOR活化情况下识别抗原后将产生全免疫应答,而在mTOR抑制情况下则产生无能.全T细胞激活伴有下游mTOR标靶S6激酶1在421位苏氨酸/424位丝氨酸磷酸化的增加以及mTOR依赖性胞膜型转铁蛋白受体(CD71)的增加.换之,无能可导致明显地S6激酶1在421位苏氨酸/424位丝氨酸磷酸化和CD71胞膜表达的减少.
相似地,逆转无能和增生无关,而与特异性mTOR活化相关.重要地是,T细胞表达人为构造的耐受雷帕霉素mTOR可对抗雷帕霉素诱导的无能.体内研究中,在正常可激发免疫反应的条件下,抑制mTOR可促使T细胞无能.另外,通过检测CD71的胞膜表达,我们能够在体内鉴别并分离无能与活化的T细胞.总之,我们的数据提示:通过整合各种环境因素, mTOR在决定抗原识别后的结果起重要作用.
2007-06-11 17:11
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xupeipei 编辑于 2007-06-21 09:27
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