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Myeloid-like B cells boost emergency myelopoiesis through IL-10 production during infection

Emergency myelopoiesis (EM) is a hematopoietic response against systemic infections that quickly supplies innate immune cells. As lymphopoiesis is strongly suppressed during EM, the role of lymphocytes in that process has not received much attention. Here, we found that myeloid-like B cells (M-B cel...

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Hauptverfasser: Kanayama, Masashi (VerfasserIn) , Izumi, Yuta (VerfasserIn) , Akiyama, Megumi (VerfasserIn) , Hayashi, Toyoki (VerfasserIn) , Atarashi, Koji (VerfasserIn) , Roers, Axel (VerfasserIn) , Sato, Taku (VerfasserIn) , Ohteki, Toshiaki (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: January 31, 2023
In: Journal of experimental medicine
Year: 2023, Jahrgang: 220, Heft: 4, Pages: 1-17, S1-S6
ISSN:1540-9538
DOI:10.1084/jem.20221221
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1084/jem.20221221
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Verfasserangaben:Masashi Kanayama, Yuta Izumi, Megumi Akiyama, Toyoki Hayashi, Koji Atarashi, Axel Roers, Taku Sato, and Toshiaki Ohteki
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Zusammenfassung:Emergency myelopoiesis (EM) is a hematopoietic response against systemic infections that quickly supplies innate immune cells. As lymphopoiesis is strongly suppressed during EM, the role of lymphocytes in that process has not received much attention. Here, we found that myeloid-like B cells (M-B cells), which express myeloid markers, emerge in the bone marrow (BM) after the induction of EM. M-B cells were mainly derived from pre-B cells and preferentially expressed IL-10, which directly stimulates hematopoietic progenitors to enhance their survival and myeloid-biased differentiation. Indeed, lacking IL-10 in B cells, blocking IL-10 in the BM with a neutralizing antibody, and deleting the IL-10 receptor in hematopoietic progenitors significantly suppressed EM, which failed to clear microbes in a cecal ligation and puncture model. Thus, a distinct B cell subset generated during infection plays a pivotal role in boosting EM, which suggests the on-demand reinforcement of EM by adaptive immune cells.
Beschreibung:Gesehen am 23.03.2023
Beschreibung:Online Resource
ISSN:1540-9538
DOI:10.1084/jem.20221221

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