Myeloid-like B cells boost emergency myelopoiesis through IL-10 production during infection
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- Masashi Kanayama
- Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University 1 , Tokyo, Japan
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- Yuta Izumi
- Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University 1 , Tokyo, Japan
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- Megumi Akiyama
- Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University 1 , Tokyo, Japan
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- Toyoki Hayashi
- Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University 1 , Tokyo, Japan
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- Koji Atarashi
- Department of Microbiology and Immunology, Keio University 2 , Tokyo, Japan
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- Axel Roers
- Institute for Immunology, Heidelberg University Hospital 3 , Heidelberg, Germany
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- Taku Sato
- Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University 1 , Tokyo, Japan
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- Toshiaki Ohteki
- Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University 1 , Tokyo, Japan
説明
<jats:p>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.</jats:p>
収録刊行物
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- Journal of Experimental Medicine
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Journal of Experimental Medicine 220 (4), 2023-01-31
Rockefeller University Press
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詳細情報 詳細情報について
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- CRID
- 1360017282238010496
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- ISSN
- 15409538
- 00221007
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- データソース種別
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- Crossref
- KAKEN