主题:Toll样受体结合通过经干扰素贝塔和蛋白激酶R诱导的吲哚胺2,3加双氧酶1增强人骨髓来源间充质干细胞的免疫抑制特性 , ^9 G9 N/ P# \$ f; q/ k/ U5 R) @ $ A8 a% k& U) }4 C说明:原文来自Stem Cell,干细胞之家新闻小组成员deron翻译(转帖请注明)+ k" D0 p* m: x' _
( I- X7 `' a' J 翻译内容:0 r$ n* a4 N9 e$ B; E# w3 L
间充质干细胞(MSC)在T细胞免疫方面具有独特的抑制特性,因而可作为一种有效手段用于治疗损伤性T细胞应答引发的相关疾病——如器官特异性自体免疫和移植物抗宿主病。Toll样受体(TLR)主要表达于抗原提呈细胞并识别保存的病原体来源组分。阻断TLR可以激活多种固有和适应性免疫应答途径,来消除和抵御侵入性病原体。本研究中,我们证明了人骨髓来源MSC表达的TLR增强了MSC的免疫抑制表型。TLR介导的免疫抑制反应不依赖于色氨酸代谢酶吲哚胺2,3加双氧酶1(IDO1)产生的免疫抑制物质犬尿氨酸。TLR诱导IDO1的反应涉及到一个自分泌的干扰素(IFN)β信号环,该信号环依赖于蛋白激酶R(PKR),并独立于IFNγ之外。这些数据赋予了TLR在MSC免疫生物学中一个新的角色,使得(生物体)在无IFNγ时增强MSC的免疫抑制特性,而非诱导促炎性免疫应答途径。PKR和IFNβ在促成MSC免疫抑制性物质犬尿氨酸的分泌上,发挥着之前未曾探明的重要作用。 3 }# m7 P$ N( ~原摘要:Mesenchymal stem cells (MSC) display unique suppressive properties on T-cell immunity, thus representing an attractive vehicle for the treatment of conditions associated with harmful T-cell responses such as organ-specific autoimmunity and graft-versus-host disease. Toll-like receptors (TLR) are primarily expressed on antigen-presenting cells and recognize conserved pathogen-derived components. Ligation of TLR activates multiple innate and adaptive immune response pathways to eliminate and protect against invading pathogens. In this work, we show that TLR expressed on human bone marrow-derived MSC enhanced the immunosuppressive phenotype of MSC. Immunosuppression mediated by TLR was dependent on the production of immunosuppressive kynurenines by the tryptophan-degrading enzyme indoleamine-2,3-dioxygenase-1 (IDO1). Induction of IDO1 by TLR involved an autocrine interferon (IFN)-β signaling loop, which was dependent on protein kinase R (PKR), but independent of IFN-γ. These data define a new role for TLR in MSC immunobiology, which is to augment the immunosuppressive properties of MSC in the absence of IFN-γ rather than inducing proinflammatory immune response pathways. PKR and IFN-β play a central, previously unidentified role in orchestrating the production of immunosuppressive kynurenines by MSC. 5 `2 |' n: E3 t. |2 U1 D) T$ i: v. W 原文:[attach]33698[/attach] 8 K- ?( g. O. ~4 q1 D0 X% D; E. @作者: deron 时间: 2011-9-24 15:29
本帖最后由 naturalkillerce 于 2011-9-25 01:11 编辑 y( ^8 M9 [: n7 x) b ?; T
5 j: p8 I/ z+ g' y" h% ^- [. z 回复 deron 的帖子 , \# O- d, h5 J6 g7 l, d 6 x+ M" M" \ T! M Immunosuppression mediated by TLR was dependent on the production of immunosuppressive kynurenines by the tryptophan-degrading enzyme indoleamine-2,3-dioxygenase-1 (IDO1). Induction of IDO1 by TLR involved an autocrine interferon (IFN)-β signaling loop, which was dependent on protein kinase R (PKR), but independent of IFN-γ. * q' z2 |3 b$ Z, y9 K/ K- K) L
楼主原译:TLR介导的免疫抑制反应不依赖于色氨酸代谢酶吲哚胺2,3加双氧酶1(IDO1)产生的免疫抑制物质犬尿氨酸。TLR诱导IDO1的反应涉及到一个自分泌的干扰素(IFN)β信号环,该信号环依赖于蛋白激酶R(PKR),并独立于IFNγ之外。 - h2 {' e! A$ e% n1 {9 a: o; }( b% }
看完原译后,我有点一头雾水,还好楼主给了英文。这里,TLR介导的免疫抑制反应是依赖于吲哚胺2,3双加氧酶1(IDO1)产生的免疫抑制物质犬尿氨酸,即“dependent on the production of immunosuppressive kynurenines”。“tryptophan-degrading enzyme”应当翻译为色氨酸降解酶。只有依赖,后面的“TLR诱导IDO1的反应”就好理解了。“ indoleamine-2,3-dioxygenase-1”应翻译为“吲哚胺2,3双加氧酶1”。还有,“ interferon (IFN)-β signaling loop”翻译为“信号环”就未免只是纯粹取字面意义了,应结合上下文理解,不然就让人看不懂了,我们知道后面提到“ protein kinase R”,说明前面讲的是细胞信号传导途径的事情,所以翻译为“干扰素β信号传导回路”或许更好一些。“independent of IFN-γ”翻译为与IFN-γ无关或许更好,前面知道TLR诱导IDO1产生需要IFN-β的参与,所以“independent of IFN-γ”就是与IFN-γ无关,即不需IFN-γ参与。 5 T" x/ H7 S6 W0 {3 |' S; \% n9 a u- e
试译:TLR介导的免疫抑制反应依赖于色氨酸降解酶吲哚胺2,3双加氧酶1(IDO1)产生的免疫抑制物质犬尿氨酸。TLR诱导IDO1产生涉及到一个自分泌的干扰素(IFN)β信号传导回路。该回路依赖于蛋白激酶R(PKR),但是不需IFN-γ参与。作者: naturalkillerce 时间: 2011-9-25 00:56
/ V1 T3 ` ]% y; h9 Q% QThese data define a new role for TLR in MSC immunobiology, which is to augment the immunosuppressive properties of MSC in the absence of IFN-γ rather than inducing proinflammatory immune response pathways. PKR and IFN-β play a central, previously unidentified role in orchestrating the production of immunosuppressive kynurenines by MSC。/ b& ?; Y! M. E1 h, R5 v4 }
楼主原译:这些数据赋予了TLR在MSC免疫生物学中一个新的角色,使得(生物体)在无IFNγ时增强MSC的免疫抑制特性,而非诱导促炎性免疫应答途径。PKR和IFNβ在促成MSC免疫抑制性物质犬尿氨酸的分泌上,发挥着之前未曾探明的重要作用。 h8 L9 W6 w$ P1 d1 b8 u9 A9 Y( U4 u5 j" V9 @& A T
这里,基本上ok啊。如果稍加润色一下,或许更好,如“这些数据赋予了TLR在MSC免疫生物学中一个新的角色,使得(生物体)在无IFNγ时增强MSC的免疫抑制特性”改为“这些数据赋予了TLR在MSC免疫生物学中一个新的角色,那就是增强无IFNγ时MSC的免疫抑制特性”。 “orchestrating”或许翻译为“协同促进"更好。即,PKR和 IFN-β在协同促进MSC产生的疫抑制性物质犬尿氨酸方面发挥着之前未曾探明的重要作用。3 C; \+ @& C$ @- Y7 R A