Figure 6.

Myelopoiesis and HSPC activation in the healthy and in conditions with chronic inflammation. In the healthy, tissue injury can induce emergency or demand-activated myelopoiesis through activation of quiescent HSCs, resulting in reactive myelopoiesis and mobilization of effector immune cells such as neutrophils and inflammatory monocytes, which typically seen in the early phase (approximately day 2). This phase is followed by timely limitation of myelopoiesis and activated HSPCs, which in turn promotes resolution of inflammation and healing. In contrast, in conditions with chronic inflammation, HSPCs are activated in a basal condition (often seen as myeloid skewing with MyP expansion). However, these activated HSPCs lack reactivity and fail quickly enough to mobilize innate immune cells, leading to nonresolution and nonhealing with sustained HSPC activation. MyP, myeloid-committed progenitor.