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Journal article

GM-CSF drives dysregulated hematopoietic stem cell activity and pathogenic extramedullary myelopoiesis in experimental spondyloarthritis

Abstract:
Dysregulated hematopoiesis occurs in several chronic inflammatory diseases, but it remains unclear how hematopoietic stem cells (HSCs) in the bone marrow (BM) sense peripheral inflammation and contribute to tissue damage. Here, we show the HSC gene expression program is biased toward myelopoiesis and differentiation skewed toward granulocyte-monocyte progenitors (GMP) during joint and intestinal inflammation in experimental spondyloarthritis (SpA). GM-CSF-receptor is increased on HSC and multipotent progenitors, favoring a striking increase in myelopoiesis at the earliest hematopoietic stages. GMP accumulate in the BM in SpA and, unexpectedly, at extramedulary sites: in the inflamed joints and spleen. Furthermore we show that GM-CSF promotes BM and extramedullary myelopoiesis, tissue-toxic neutrophil accumulation in target organs, and GM-CSF prophylactic or therapeutic blockade substantially decreases SpA severity. Surprisingly, besides CD4 T cells and innate lymphoid cells, mast cells (MC) are a source of GM-CSF in inflammation, and its pathogenic production is promoted by the alarmin IL-33.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1038/s41467-019-13853-4

Authors


More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
NDORMS
Role:
Author
More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
NDORMS
Role:
Author
More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
NDORMS
Role:
Author
More by this author
Institution:
University of Oxford
Division:
Medical Sciences Division
Department:
NDORMS
Role:
Author


Publisher:
Nature Research
Journal:
Nature Communications More from this journal
Volume:
11
Issue:
2020
Article number:
155
Publication date:
2020-01-09
Acceptance date:
2019-12-02
DOI:
ISSN:
2041-1723


Pubs id:
pubs:1081263
UUID:
uuid:d3dd80bb-30db-44f2-842b-6f7abc151f02
Local pid:
pubs:1081263
Source identifiers:
1081263
Deposit date:
2020-01-08

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