ArticleStem cell reports2022
Neutrophils as regulators of macrophage-induced inflammation in a setting of allogeneic bone marrow transplantation.
Article in Stem cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Clonal dynamics, tolerance, and adverse events after CD45-ADC-conditioned autologous HSPC transplantation in macaques.Blood advances · 2026Article
- Review
- Immune-mediated mechanisms in acute osteofascial compartment syndrome: insights from multi-omics analysis.European journal of medical research · 2025Article
- Advances in research on the role of neutrophils in organ transplant rejection.Frontiers in immunology · 2025Review
- A superior tool for predicting sepsis in SAH patients: The nomogram outperforms SOFA score.PloS one · 2025Article
- Unraveling devitalization: its impact on immune response and ectopic bone remodeling from autologous and allogeneic callus mimics.Stem cells translational medicine · 2024Article
- Improvement of the sepsis survival rate by adenosine 2a receptor antagonists depends on immune regulatory functions of regulatory T-cells.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clinical data reveal that patients with allogeneic hematopoietic stem cell transplantation (HSCT) are vulnerable to infection and prone to developing severe sepsis, which greatly compromises the success of transplantation, indicating a dysregulation of inflammatory immune response in this clinical setting. Here, by using a mouse model of haploidentical bone marrow transplantation (haplo-BMT), we found that uncontrolled macrophage inflammation underlies the pathogenesis of both LPS- and E.coli-induced sepsis in recipient animals with graft-versus-host disease (GVHD). Deficient neutrophil maturation in GVHD mice post-haplo-BMT diminished modulation of macrophage-induced inflammation, which was mechanistically dependent on MMP9-mediated activation of TGF-β1. Accordingly, adoptive transfer of mature neutrophils purified from wild-type donor mice inhibited both sterile and infectious sepsis in GVHD mice post-haplo-BMT. Together, our findings identify a novel mature neutrophil-dependent regulation of macrophage inflammatory response in a haplo-BMT setting and provide useful clues for developing clinical strategies for patients suffering from post-HSCT sepsis.
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