Dendritic cells (DCs) are first in line to sense invading microbes and to deliver signals to other immune cells. Plasmacytoid DCs (pDC) produce high amounts of type I interferons (IFNs) but also regulate immune responses. Using the Clec4C (BDCA2)‐diphtheria toxin receptor mouse model allowing conditional pDC depletion, we identified an essential role for pDCs in regulating intestinal inflammation locally in the gut. In pDC‐depleted mice, Citrobacter rodentium infection led to enhanced activation of conventional DCs and induction of IFN‐γ‐producing Th1‐cells in colon‐draining lymph nodes, while induction of Foxp3⁺/CD25⁺ Treg and IL‐17‐producing Th17 cells was impaired. Concomitantly, F4/80⁺ macrophages accumulated into the colon lamina propria in excess, and levels of Il‐1β and Tnf transcripts increased and Foxp3⁺ Treg were fewer. Our results indicate that pDCs control inflammation in the gut during C. rodentium infection and that they have an important immune regulatory role in colon‐draining lymph nodes.

中文翻译：

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浆细胞样树突状细胞调节宿主对柠檬酸杆菌引起的结肠引流淋巴结结肠炎的免疫反应

树突状细胞 (DC) 是首先感知入侵微生物并将信号传递给其他免疫细胞的人。浆细胞样 DC (pDC) 产生大量 I 型干扰素 (IFN)，但也调节免疫反应。使用允许条件性 pDC 耗竭的Clec4C (BDCA2)-白喉毒素受体小鼠模型，我们确定了 pDC 在调节肠道局部肠道炎症中的重要作用。在 pDC 耗尽的小鼠中，柠檬酸杆菌感染导致常规 DC 的激活增强和结肠引流淋巴结中产生 IFN-γ 的 Th1 细胞的诱导，同时诱导 Foxp3 ⁺ /CD25 ⁺ Treg 和产生 IL-17 的 Th17细胞受损。同时，F4/80 ⁺巨噬细胞过量积聚到结肠固有层，Il-1β 和 Tnf 转录物水平增加，Foxp3 ⁺ Treg 减少。我们的结果表明，pDCs 在啮齿类动物感染期间控制肠道炎症，并且它们在结肠引流淋巴结中具有重要的免疫调节作用。