ArticleBlood advances2020
Runx1 negatively regulates inflammatory cytokine production by neutrophils in response to Toll-like receptor signaling.
Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 78 citations in OpenAlex.
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- Single-cell transcriptomic unveils tumor-mediated reprogramming of neutrophils and their unique vulnerability that inhibits metastasis.Science advances · 2026Article
- Clonal lineage tracing of innate immune cells in human cancer.Cancer cell · 2026Article
- Cellular architecture and neighborhood-informed virtual spatial tumor profiling from histopathology.Cell · 2026Article
- Runx1-Snx9 axis drives the pathological secretion of mitochondrial-derived vesicles to activate cGAS-STING signaling in acute pancreatitis.Journal of nanobiotechnology · 2026Article
- Common ancestral origin of indeterminate dendritic cell tumor and chronic myelomonocytic leukemia in clonal hematopoiesis.Haematologica · 2026Article
- Circulating microRNAs miR-21-5p, miR-23a-3p and miR-26a-5p reflect clinical and molecular features of aging.Scientific reports · 2025Article
- Targeting RUNX1 Germline Variants: Agents Under Investigation.Current hematologic malignancy reports · 2025Review
- The Dual Role of RUNX1 in Inflammation-Driven Age-Related Diseases: From Molecular Mechanisms to Clinical Translation.Biomedicines · 2025Review
- An inflammatory T-cell-stromal axis contributes to hematopoietic stem/progenitor cell failure and clonal evolution in human myelodysplastic syndrome.Nature communications · 2025Article
- GATA2 decommissioning of enhancers: A mechanism to constrain inflammatory signaling.Cell reports · 2025Article
- CBFβ-SMMHC-driven leukemogenesis requires enhanced RUNX1-DNA binding affinity in mice.The Journal of clinical investigation · 2025Article
- Insights into the clinical, platelet and genetic landscape of inherited thrombocytopenia with malignancy risk.British journal of haematology · 2025Article
- Hereditary Hematopoietic Malignancies: Considerations for Optimizing Diagnosis and Management.Current oncology reports · 2025Review
- Whole Transcriptome RNA-Seq Reveals Drivers of Pathological Dysfunction in a Transgenic Model of Alzheimer's Disease.Molecular neurobiology · 2025Article
- African swine fever virus infection enhances CD14-dependent phagocytosis of porcine alveolar macrophages to promote bacterial uptake and apoptotic body-mediated viral transmission.Journal of virology · 2025Article
- Dual mechanism of inflammation sensing by the hematopoietic progenitor genome.Science advances · 2025Article
- Targeting the CD74 signaling axis suppresses inflammation and rescues defective hematopoiesis inScience translational medicine · 2025Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
RUNX1 is frequently mutated in myeloid and lymphoid malignancies. It has been shown to negatively regulate Toll-like receptor 4 (TLR4) signaling through nuclear factor κB (NF-κB) in lung epithelial cells. Here we show that RUNX1 regulates TLR1/2 and TLR4 signaling and inflammatory cytokine production by neutrophils. Hematopoietic-specific RUNX1 loss increased the production of proinflammatory mediators, including tumor necrosis factor-α (TNF-α), by bone marrow neutrophils in response to TLR1/2 and TLR4 agonists. Hematopoietic RUNX1 loss also resulted in profound damage to the lung parenchyma following inhalation of the TLR4 ligand lipopolysaccharide (LPS). However, neutrophils with neutrophil-specific RUNX1 loss lacked the inflammatory phenotype caused by pan-hematopoietic RUNX1 loss, indicating that dysregulated TLR4 signaling is not due to loss of RUNX1 in neutrophils per se. Rather, single-cell RNA sequencing indicates the dysregulation originates in a neutrophil precursor. Enhanced inflammatory cytokine production by neutrophils following pan-hematopoietic RUNX1 loss correlated with increased degradation of the inhibitor of NF-κB signaling, and RUNX1-deficient neutrophils displayed broad transcriptional upregulation of many of the core components of the TLR4 signaling pathway. Hence, early, pan-hematopoietic RUNX1 loss de-represses an innate immune signaling transcriptional program that is maintained in terminally differentiated neutrophils, resulting in their hyperinflammatory state. We hypothesize that inflammatory cytokine production by neutrophils may contribute to leukemia associated with inherited RUNX1 mutations.
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