Mature B cells and mesenchymal stem cells control emergency myelopoiesis

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<jats:p>Systemic inflammation halts lymphopoiesis and prioritizes myeloid cell production. How blood cell production switches from homeostasis to emergency myelopoiesis is incompletely understood. Here, we show that lymphotoxin-β receptor (LTβR) signaling in combination with TNF and IL-1 receptor signaling in bone marrow mesenchymal stem cells (MSCs) down-regulates<jats:italic>Il7</jats:italic>expression to shut down lymphopoiesis during systemic inflammation. LTβR signaling in MSCs also promoted CCL2 production during systemic inflammation. Pharmacological or genetic blocking of LTβR signaling in MSCs partially enabled lymphopoiesis and reduced monocyte numbers in the spleen during systemic inflammation, which correlated with reduced survival during systemic bacterial and viral infections. Interestingly, lymphotoxin-α1β2 delivered by B-lineage cells, and specifically by mature B cells, contributed to promote<jats:italic>Il7</jats:italic>down-regulation and reduce MSC lymphopoietic activity. Our studies revealed an unexpected role of LTβR signaling in MSCs and identified recirculating mature B cells as an important regulator of emergency myelopoiesis.</jats:p>
Publisher
LIFE SCIENCE ALLIANCE LLC
Issue Date
2023-04
Language
English
Article Type
Article
Citation

LIFE SCIENCE ALLIANCE, v.6, no.4

ISSN
2575-1077
DOI
10.26508/lsa.202301924
URI
http://hdl.handle.net/10203/306076
Appears in Collection
MSE-Journal Papers(저널논문)
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