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. 2019 Feb 7;10:172. doi: 10.3389/fimmu.2019.00172

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Copyright © 2019 Wang, Ding, Guo and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Primary tumors promote the mobilization of MDSCs from bone marrow to secondary sites. (A) At primary tumor site, tumor or stromal cells secrete numerous cytokines and EVs that are systemically distributed following the blood circulation. (B) In the bone marrow (BM), cytokines, such as macrophage-colony stimulating factor (M-CSF), granulocyte macrophage-colony stimulating factor (GM-CSF), interleukin 6 (IL-6), interferon gamma (IFN-γ), vascular endothelial growth factor (VEGF) from primary tumors promote MDSCs differentiation from granulocyte/monocyte precursor (GMP). Moreover, these cytokines mobilize MDSCs into the bloodstream through enhancing actin polymerization and vascular leakiness. (C) Cytokines from primary tumors, such as chemokine (C-X-C motif) ligand 1 (CXCL1), chemokine (CC motif) ligand 12 (CCL12), chemokine (CC motif) ligand 2 (CCL2), chemokine (CC motif) ligand 15 (CCL15), matrix metalloproteinases (MMPs), S100A8/A9, and tumor necrosis factor α (TNF-α) guide the homing of MDSCs to in secondary sites through chemotaxis and enhancin vascular remodeling, which create conditions conducive for MDSC mobilization to PMN. Moreover, factors or exosomes from primary tumor also enhance progenitors mobilization to the PMN and these progenitors further differentiate into MDSCs.