De-stressing the T cells in need.
De-stressing the T cells in need.
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为需要的 T 细胞减压。
DOI：
10.1126/science.abi7265
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Dutta,Anindya
中科院分区：
文献类型：
--
作者：
Su,Zhangli;Dutta,Anindya
当暴露于外部抗原时，T细胞迅速活化以增殖和分化。一项遗传筛查发现了一种称为delektra的突变，该突变通过Schlafen 2（Slfn2）基因中的单一功能丧失错义突变导致小鼠免疫缺陷（1）。Slfn2突变与受损的T细胞活化相关。然而，Slfn2是否直接调节T细胞功能，以及如何调节，尚不清楚。第703页，Yue et al. (2)报道，SLFN 2保护T细胞在活化过程中免受过度应激，从而促进蛋白质翻译的必要上调。SLFN 2结合并屏蔽转移RNA（tRNA），信使RNA（mRNA）翻译中的必需衔接分子，使其免受应激激活的片段化。在没有SLFN 2的情况下，过度的tRNA片段化降低了整体翻译，并特别降低了对T细胞活化重要的关键细胞因子受体蛋白的翻译。这项研究扩展了tRNA片段化的作用，并暗示SLFN 2在防止片段化以实现免疫功能中的作用。
When exposed to external antigens, T cells are rapidly activated to proliferate and differentiate. A genetic screen identified a mutation calledelektrathat causes immunodeficiency in mice through a single loss-of-function missense mutation in the Schlafen 2 (Slfn2) gene (1).Slfn2mutation was associated with impaired T cell activation. However, whetherSlfn2regulates T cell function directly, and how, was unclear. On page 703 of this issue, Yueet al.(2) report that SLFN2 safeguards T cells from excessive stress during activation and thus facilitates the necessary up-regulation of protein translation. SLFN2 binds and shields transfer RNAs (tRNAs), essential adaptor molecules in translation of messenger RNAs (mRNAs), from stress-activated fragmentation. Without SLFN2, excessive tRNA fragmentation lowers global translation and specifically decreases the translation of key cytokine receptor proteins important for T cell activation. This study expands the role of tRNA fragmentation and implicates SLFN2 in preventing fragmentation to enable immune function.