Megumi Akiyama
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Megumi Akiyama has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Axel Roers
Institute for Immunology, Heidelberg University Hospital, Heidelberg, Germany
1 shared publication - Koji Atarashi
Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan
1 shared publication - Masashi Kanayama
Division of Molecular Immunology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan
1 shared publication - Taku Sato
Department of Biochemistry and Molecular Biology, Nippon Medical School Graduate School of Medicine, Tokyo 113-8603, Japan
1 shared publication - Toshiaki Ohteki
Institute of Science Tokyo
1 shared publication - Toyoki Hayashi
Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University 1 , Tokyo, Japan
1 shared publication
Latest Publications
- Open Access
- 31 January 2023
- Published by Rockefeller University Press in Journal of Experimental Medicine
- Vol. 220 (4)
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 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.
- 31 January 2023
- Published by Rockefeller University Press in Journal of Experimental Medicine
- Vol. 220 (4)
Open AccessMyeloid-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 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.