慢性炎性脱髓鞘性多发性神经根神经病（CIDP）为最常见的慢性可治性周围神经病，其发病原因主要为针对自身的异常免疫反应导致周围神经髓鞘和轴索损害。有文献报道CIDP患者的调节性T细胞（Treg）的抑制功能有所减低，然而其上游通路如何，以及如何选择性的恢复Treg细胞的抑制功能，来清除病理性的T细胞，尚未有研究涉及。我们拟测定CIDP患者的Treg细胞中，雷帕霉素的机械靶点复合物（mTORC）的活性是否较正常人异常增高；CIDP的Treg对于效应T细胞的抑制功能、以及抑制性细胞因子的分泌是否有所减退；若CIDP的mTOR通路存在过度激活，通过雷帕霉素抑制mTOR通路的过度激活，是否可以恢复Treg细胞的免疫调节功能。通过研究CIDP患者中调节Treg细胞分化的上游-mTOR通路的激活状态，以及雷帕霉素对于选择性的恢复Treg细胞的免疫调节功能的作用，我们希望为CIDP的特异性治疗提供新的思路。

As the most common treatable chronic neuropathy, chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an autoimmune disorder in which aberrant immune response is directed towards components of the peripheral nerve causing demyelination and axonal damage. There’s report about the decreased inhibitory function of regulatory T (Treg) cells in CIDP patients. However, no researches have looked into the upstream pathway, or how the decreased inhibitory function of Treg cells could be restored to eliminate pathological T cells..In our research, we intend to answer the following questions: whether the mechanistic target of rapamycin complex 1 (mTORC1) and mTORC2 are over-activated in Treg cells of CIDP compared with health control; whether the inhibitory function and secretion of inhibitory cytokines are impaired in Tregs of CIDP patients; and if the mTOR is over-activated in Tregs of CIDP paitents, whether rapamycin could restore the immune-modulatory function of Treg cells through inhibition of mTOR. .By analyzing the activation status of mTOR in CIDP, which is the upstream regulator of Treg differentiation, as well as applying rapamycin to selectively restore the immune-modulatory function of Treg cells, we intend to find novel ways for the specific treatment for CIDP.