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. Collaboration between myeloid and lymphoid lineages on hematopoiesis has not been fully elucidated. Here, we showed that during systemic infection, a unique B cell subset expressing myeloid markers emerged to enhance on-demand emergency myelopoiesis by producing IL-10.

Automated summary

Emergency myelopoiesis is a hematopoietic response against systemic infections, but the role of lymphocytes in this process has not received much attention. This study found that a unique B cell subset expressing myeloid markers emerged in the bone marrow during emergency myelopoiesis, and these cells preferentially expressed IL-10, which stimulated hematopoietic progenitors for enhanced myeloid differentiation. Blocking IL-10 significantly suppressed emergency myelopoiesis and hindered microbial clearance in a model of cecal ligation and puncture. These findings suggest the importance of adaptive immune cells in boosting emergency myelopoiesis.