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

DOI PDF 参考文献64件 オープンアクセス
  • Masashi Kanayama
    Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University 1 , Tokyo, Japan
  • Yuta Izumi
    Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University 1 , Tokyo, Japan
  • Megumi Akiyama
    Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University 1 , Tokyo, Japan
  • Toyoki Hayashi
    Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University 1 , Tokyo, Japan
  • Koji Atarashi
    Department of Microbiology and Immunology, Keio University 2 , Tokyo, Japan
  • Axel Roers
    Institute for Immunology, Heidelberg University Hospital 3 , Heidelberg, Germany
  • Taku Sato
    Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University 1 , Tokyo, Japan
  • Toshiaki Ohteki
    Department of Biodefense Research, Medical Research Institute, Tokyo Medical and Dental University 1 , Tokyo, Japan

抄録

<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>

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