Innate immune cellular effectors are actively consumed during systemic inflammation but the systemic traffic and the mechanisms that support their replenishment remain unknown. Here we demonstrate that acute systemic inflammation induces the emergent activation of a previously unrecognized system of rapid migration of granulocyte-macrophage progenitors and committed macrophage-dendritic progenitors, but not other progenitors or stem cells, from bone marrow (BM) to lymphatic capillaries. The progenitor traffic to the systemic lymphatic circulation is mediated by Ccl19/Ccr7 and is NFκB independent, Traf6/IκB-kinase/SNAP23 activation which is responsible for the secretion of pre-stored Ccl19 by a subpopulation of CD205+/CD172a+ conventional dendritic cells type 2 (cDC2) and upregulation of BM myeloid progenitor Ccr7 signaling. The consequence of this progenitor traffic is anti-inflammatory with promotion of early survival and initiation of replenishment of lymph node cDC.

中文翻译：

---

全身性炎症从BM募集速效抗炎先天性骨髓祖细胞进入淋巴管

先天性免疫细胞效应子在全身性炎症过程中被活跃地消耗，但是全身性运输及其支持其补充的机制仍然未知。在这里，我们证明了急性全身性炎症诱发了先前未被认可的粒细胞-巨噬细胞祖细胞和定型巨噬细胞-树突祖细胞（而不是其他祖细胞或干细胞）从骨髓（BM）到淋巴毛细血管的快速迁移的紧急激活。祖细胞进入系统淋巴循环是由Ccl19 / Ccr7介导的，并且是NFκB独立的Traf6 /IκB激酶/ SNAP23激活，负责通过CD205 + / CD172a + 2型常规树突状细胞亚群分泌预存的Ccl19。 （cDC2）和BM骨髓祖细胞Ccr7信号转导上调。