| First Author | Ikeda N | Year | 2023 |
| Journal | Cell Rep | Volume | 42 |
| Issue | 3 | Pages | 112165 |
| PubMed ID | 36862552 | Mgi Jnum | J:334881 |
| Mgi Id | MGI:7463851 | Doi | 10.1016/j.celrep.2023.112165 |
| Citation | Ikeda N, et al. (2023) The early neutrophil-committed progenitors aberrantly differentiate into immunoregulatory monocytes during emergency myelopoiesis. Cell Rep 42(3):112165 |
| abstractText | Inflammatory stimuli cause a state of emergency myelopoiesis leading to neutrophil-like monocyte expansion. However, their function, the committed precursors, or growth factors remain elusive. In this study we find that Ym1(+)Ly6C(hi) monocytes, an immunoregulatory entity of neutrophil-like monocytes, arise from progenitors of neutrophil 1 (proNeu1). Granulocyte-colony stimulating factor (G-CSF) favors the production of neutrophil-like monocytes through previously unknown CD81(+)CX3CR1(lo) monocyte precursors. GFI1 promotes the differentiation of proNeu2 from proNeu1 at the cost of producing neutrophil-like monocytes. The human counterpart of neutrophil-like monocytes that also expands in response to G-CSF is found in CD14(+)CD16(-) monocyte fraction. The human neutrophil-like monocytes are discriminated from CD14(+)CD16(-) classical monocytes by CXCR1 expression and the capacity to suppress T cell proliferation. Collectively, our findings suggest that the aberrant expansion of neutrophil-like monocytes under inflammatory conditions is a process conserved between mouse and human, which may be beneficial for the resolution of inflammation. |
