Cited by 423Neutrophil, Myeloperoxidase and Oxidative MechanismsWound Healing and TreatmentsInflammation biomarkers and pathways

More friend than foe: the emerging role of neutrophils in tissue repair

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Peiseler, Moritz, Kubes, Paul·2019·Journal of Clinical Investigation

Abstract

Neutrophils are the most abundant immune cells in humans and serve as first responders to a myriad of host perturbations. Equipped with a plethora of antimicrobial molecules, neutrophils invade sites of inflammation to eradicate pathogens and clear debris. Traditionally, neutrophils were thought to cause collateral tissue damage before dying at the site. However, the presence of neutrophil infiltration into sterile injuries (in the absence of infections) suggests additional roles for these cells. Now, the view of neutrophils as indiscriminate killers seems to be changing as evolving evidence suggests that neutrophils actively orchestrate resolution of inflammation and contribute to tissue repair. Novel concepts include the idea that neutrophils are key to revascularization and subsequently reverse-transmigrate back to the vasculature, actively leaving sites of tissue damage to re-home to functional niches in the lung and bone marrow. This Review scrutinizes the role of neutrophils in tissue damage and repair, discussing recent findings and raising unresolved questions around this intriguing immune cell.

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  • The observation of CD66b+ cells is consistent with VO differentiation of unique immune cell types that support vascular function.

    “Considering the immune cells are predominantly myeloid‐derived, the observation of CD66b+ cells is consistent with VO differentiation of unique immune cell types that support vascular function.[ 8 , 84 , 85 ]”

    From Coordinated Development of Immune Cell Populations in Vascularized Skin Organoids from Human Induced Pluripotent Stem Cells (2025) · cites this paper as [84]

    The “Neutrophils in tissue repair” section describes a proangiogenic neutrophil subset and reports that neutrophils promote revascularization, supporting the vascular-function rationale. It does not identify CD66b+ cells or address differentiation in VOs, so it cannot substantiate that specific interpretation. (LLM, conf=0.84)

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Sorted by citations

Authors
Peiseler, M., & Kubes, P.
Affiliations
University of Calgary (CA)
Venue
Journal of Clinical Investigation
Published
2019-06-17
Volume
129
Issue
7
Pages
2629-2639
ISSN
  • 0021-9738 (ISSN-L)
  • 1558-8238
OpenAlex
W2952553905
Cited by
423
References
13
Citations by year
2026: 64 · 2025: 79 · 2024: 87 · 2023: 55 · 2022: 62 · 2021: 49 · 2020: 22 · 2019: 5
FWCI
2.97
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Heart and Stroke Foundation of Canada
  • Deutsche Forschungsgemeinschaft (PE2737/1-1)
  • Canada Research Chairs
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords
neutrophils, tissue repair, inflammation resolution, sterile inflammation, tissue damage, neutrophil heterogeneity
MeSH terms
Animals, Humans, Inflammation, Neutrophils, Regeneration, Neutrophil Infiltration

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