I read the article by Zhang et al. published in this journal with great interest (1). They demonstrated that CD4⁺ T cells isolated from Takayasu's arteritis (TAK) are biased to differentiate into Th1 and Th17 cells because of mechanistic target of rapamycin complex 1 (mTORC1) hyperactivity. Subsequently, using human artery‐NSG chimera model, they showed that mTORC1 inhibition, by either rapamycin or RNAi technology, effectively abrogated the mal‐differentiation of TAK CD4⁺ T cells and vascular inflammation.

中文翻译：

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CD4 + T细胞在高津市大动脉炎免疫病理学中的关键作用：评论文章作者。

我读了张等人的文章。在本杂志上发表的文章引起了极大的兴趣（1）。他们证明，由于雷帕霉素复合物1（mTORC1）过度活跃的机制靶点，从高津市大动脉炎（TAK）分离出的CD4 ⁺ T细胞倾向于分化为Th1和Th17细胞。随后，他们使用人动脉-NSG嵌合体模型显示，雷帕霉素或RNAi技术抑制mTORC1可有效消除TAK CD4 ⁺ T细胞的分化不良和血管炎症。