Immune regulation through dendritic cell-specific mTOR pathway

尽管一些报道表明mTORC1参与树突状细胞（dc）的发育和功能，但其生理作用仍不清楚。通过使用mTORC1信号缺失的小鼠，特别是在DC谱系中（这里称为RaptorDC-/-），我们发现mTORC1信号受损导致肠道CD11c+CD11b+ DC中IL-10的产生受到抑制。Raptor是mTORC1信号的重要组成部分。我们还发现RaptorDC-/-小鼠对葡聚糖硫酸钠诱导的结肠炎高度敏感。

Although several reports have suggested the involvement of mTORC1 in development and function of dendritic cells (DCs), its physiological roles remain obscure. By using mTORC1 signal-deficient mice lacking Raptor, an essential component of mTORC1 signal, specifically in DC lineage (referred to here as RaptorDC-/-), we found that impaired mTORC1 signal resulted in the suppression of IL-10 production in intestinal CD11c+CD11b+ DCs. We also found that RaptorDC-/- mice were highly susceptible to dextran sodium sulfate-induced colitis.