In response to the points raised by Luo et al., first, we agree that focusing on the IL-6-JAK2-STAT3 pathway may overlook some other drivers of maladaptive emergency granulopoiesis (EG) and that damage-associated molecular patterns (DAMPs), such as S100A8/A9 produced and secreted by myeloid-derived suppressor cells (MDSCs), may perpetuate maladaptive EG. Thus, activation of the JAK2-STAT3 axis, which is seen in our patients with poor outcomes and is a major driver of EG,1 may have been elicited by another granulopoietic cytokine, such as G-CSF, which is elevated in these patients, or by cytokines that were not measured in our study (e.g.
In response to the points raised by Luo et al., first, we agree that focusing on the IL-6-JAK2-STAT3 pathway may overlook some other drivers of maladaptive emergency granulopoiesis (EG) and that damage-associated molecular patterns (DAMPs), such as S100A8/A9 produced and secreted by myeloid-derived suppressor cells (MDSCs), may perpetuate maladaptive EG. Thus, activation of the JAK2-STAT3 axis, which is seen in our patients with poor outcomes and is a major driver of EG,1 may have been elicited by another granulopoietic cytokine, such as G-CSF, which is elevated in these patients, or by cytokines that were not measured in our study (e.g.