| Autor: |
Naoki Ikeda, Hiroaki Kubota, Risa Suzuki, Mitsuki Morita, Ayana Yoshimura, Yuya Osada, Keigo Kishida, Daiki Kitamura, Ayaka Iwata, Satoshi Yotsumoto, Daisuke Kurotaki, Koutarou Nishimura, Akira Nishiyama, Tomohiko Tamura, Takashi Kamatani, Tatsuhiko Tsunoda, Miyako Murakawa, Yasuhiro Asahina, Yoshihiro Hayashi, Hironori Harada, Yuka Harada, Asumi Yokota, Hideyo Hirai, Takao Seki, Makoto Kuwahara, Masakatsu Yamashita, Shigeyuki Shichino, Masato Tanaka, Kenichi Asano |
| Jazyk: |
angličtina |
| Rok vydání: |
2023 |
| Předmět: |
|
| Zdroj: |
Cell Reports, Vol 42, Iss 3, Pp 112165- (2023) |
| Druh dokumentu: |
article |
| ISSN: |
2211-1247 |
| DOI: |
10.1016/j.celrep.2023.112165 |
| Popis: |
Summary: 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+Ly6Chi 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+CX3CR1lo 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. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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