With great interest, we read the commentary by Dr. Ryu Watanabe. This commentary highlights the main findings of our recent study that demonstrates the biased mal‐differentiation of Th1 and Th17 cells in patients with Takayasu's arteritis (TAK) and identifies mTORC1 hyperactivity as the T cell‐intrinsic mechanism [1]. Accordingly, targeting mTORC1 efficiently abrogates the pro‐inflammatory T cell differentiation and ameliorates arterial inflammation in humanized TAK model [1].

中文翻译：

---

回复。

我们怀着极大的兴趣阅读了渡边龙博士的评论。这篇评论强调了我们最近的研究的主要发现，该发现证明了Takayasu动脉炎（TAK）患者Th1和Th17细胞的偏向分化，并确定mTORC1过度活跃是T细胞的内在机制[1]。因此，在人源化TAK模型中，靶向mTORC1可有效消除促炎性T细胞分化并改善动脉炎症[1]。