Myeloid cells promote interferon signaling-associated deterioration of the hematopoietic system

Jacqueline Feyen, Zhen Ping, Lanpeng Chen, Claire Dijk, Tim V. D. Tienhoven, Paulina M. H. Strien, Remco M. Hoogenboezem, Michiel J. W. Wevers, Mathijs A. Sanders, Ivo P. Touw and Marc H. G. P. Raaijmakers ()
Additional contact information
Jacqueline Feyen: Erasmus MC Cancer Institute
Zhen Ping: Erasmus MC Cancer Institute
Lanpeng Chen: Erasmus MC Cancer Institute
Claire Dijk: Erasmus MC Cancer Institute
Tim V. D. Tienhoven: Erasmus MC Cancer Institute
Paulina M. H. Strien: Erasmus MC Cancer Institute
Remco M. Hoogenboezem: Erasmus MC Cancer Institute
Michiel J. W. Wevers: Erasmus MC Cancer Institute
Mathijs A. Sanders: Erasmus MC Cancer Institute
Ivo P. Touw: Erasmus MC Cancer Institute
Marc H. G. P. Raaijmakers: Erasmus MC Cancer Institute

Nature Communications, 2022, vol. 13, issue 1, 1-15

Abstract: Abstract 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.

Date: 2022
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DOI: 10.1038/s41467-022-35318-x

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