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. Author manuscript; available in PMC: 2022 Dec 1.
Published in final edited form as: Curr Opin Immunol. 2021 Aug 16;73:16–24. doi: 10.1016/j.coi.2021.07.007

Figure 1: Bone marrow myelopoiesis during inflammation.

Figure 1:

A) Development of DC-like and neutrophil-like monocytes in the bone marrow. HSCs and MPPs generate CMPs that are committed to the myeloid lineage, at which point monocyte development pathways diverge. CMPs can differentiate into MDPs that generate cMOPs, that in turn make DC-like monocytes. CMPs can also differentiate into GMPs that generate MPs, which then make neutrophil-like monocytes. In vivo treatment with LPS promotes the development of DC-like monocytes, whereas treatment with CpG DNA promotes the development of neutrophil-like monocytes. B) Emergency myelopoiesis promotes myelopoiesis over lymphopoiesis in response to infection or inflammation. This can be via direct signals, such as TLRs, on HSCs, MPPs, or CMPs or via indirect signals, such as cytokines made by other cells or progenitors themselves. C) In a zebrafish model, caspase-1 activation in HSCs caused the cleavage of GATA-1, a key transcription factor promoting megakaryocyte and erythrocyte development, leading to increased output of monocytes and neutrophils and reduced megakaryocytes and erythrocytes.