造血
髓样
生物
先天免疫系统
干细胞
祖细胞
细胞生物学
骨髓
造血干细胞
免疫学
免疫系统
作者
Jacqueline Feyen,Zhen Ping,Lanpeng Chen,Claire van Dijk,Tim van Tienhoven,Paulina M. H. van Strien,Remco M. Hoogenboezem,Michiel J. W. Wevers,Mathijs A. Sanders,Ivo P. Touw,Marc H.G.P. Raaijmakers
标识
DOI:10.1038/s41467-022-35318-x
摘要
Innate and adaptive immune cells participate in the homeostatic regulation of hematopoietic stem cells (HSCs). Here, we interrogate the contribution of myeloid cells, the most abundant cell type in the mammalian bone marrow, in a clinically relevant mouse model of neutropenia. Long-term genetic depletion of neutrophils and eosinophils results in activation of multipotent progenitors but preservation of HSCs. Depletion of myeloid cells abrogates HSC expansion, loss of serial repopulation and lymphoid reconstitution capacity and remodeling of HSC niches, features previously associated with hematopoietic aging. This is associated with mitigation of interferon signaling in both HSCs and their niches via reduction of NK cell number and activation. These data implicate myeloid cells in the functional decline of hematopoiesis, associated with activation of interferon signaling via a putative neutrophil-NK cell axis. Innate immunity may thus come at the cost of system deterioration through enhanced chronic inflammatory signaling to stem cells and their niches.
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