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. 2019 Sep 4;10:2055. doi: 10.3389/fimmu.2019.02055

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Copyright © 2019 Hamilton.

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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GM-CSF and monocytes/macrophages in inflammation. Depicted are some potential local and systemic actions of GM-CSF on monocyte/macrophage populations during an inflammatory reaction. Whether particular actions operate are currently debated and are likely to depend on the nature of the inflammatory reaction and the levels of GM-CSF attained from hemopoietic (e.g., lymphocyte) and non-hemopoietic (e.g., fibroblast) cell populations. Locally GM-CSF can act in a concentration—dependent manner on target cells (resident macrophages and/or blood-derived monocytes) to promote their survival and/or polarization/differentiation; the latter cell target can give rise to MoDCs. Their polarization/differentiation can be characterized by the production of proinflammatory mediators such as cytokines (e.g., IL-1β, TNF), proteases, reactive oxygen species (ROS), etc. One interesting pathway (zoomed), which seems to be important for GM-CSF-dependent inflammation and associated pain, leads to CCL17 production via JMJD3 and IRF4. GM-CSF can also act systemically in the blood and/or bone marrow, either directly or indirectly () via its cellular targets in the tissue, leading to migration/mobilization of monocytes or their precursors and/or monocyte development from these precursors (myelopoiesis) (). MoDC, monocyte-derived DC.

Inline graphic — GM-CSF and monocytes/macrophages in inflammation. Depicted are some potential local and systemic actions of GM-CSF on monocyte/macrophage populations during an inflammatory reaction. Whether particular actions operate are currently debated and are likely to depend on the nature of the inflammatory reaction and the levels of GM-CSF attained from hemopoietic (e.g., lymphocyte) and non-hemopoietic (e.g., fibroblast) cell populations. Locally GM-CSF can act in a concentration—dependent manner on target cells (resident macrophages and/or blood-derived monocytes) to promote their survival and/or polarization/differentiation; the latter cell target can give rise to MoDCs. Their polarization/differentiation can be characterized by the production of proinflammatory mediators such as cytokines (e.g., IL-1β, TNF), proteases, reactive oxygen species (ROS), etc. One interesting pathway (zoomed), which seems to be important for GM-CSF-dependent inflammation and associated pain, leads to CCL17 production via JMJD3 and IRF4. GM-CSF can also act systemically in the blood and/or bone marrow, either directly or indirectly () via its cellular targets in the tissue, leading to migration/mobilization of monocytes or their precursors and/or monocyte development from these precursors (myelopoiesis) (). MoDC, monocyte-derived DC.