ArticleNature immunology2024
An IL-1β-driven neutrophil-stromal cell axis fosters a BAFF-rich protumor microenvironment in individuals with multiple myeloma.
Article in Nature immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Bone Marrow Microenvironment Drives Mature Neutrophil to a CD83International journal of cancer · 2026Article
- Targeting ARF6-SUCNR1 Axis: Antisense Oligonucleotide Adjuvants for Neutrophil Immunometabolism.International journal of molecular sciences · 2026Review
- SSR4 Sustains Tertiary Lymphoid Structures by Regulation Quality Control of N-linked Glycosylation During B-cell Differentiation Into Plasmacyte in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Stromal and endothelial transcriptional changes during progression from MGUS to myeloma and after treatment response.Nature communications · 2026Article
- Engineering bone marrow in a dish-a bloody business: preclinical opportunities, translational use cases, and a call for consensus.Journal of thrombosis and haemostasis : JTH · 2026Review
- Spatial single-cell landscape of tumor-associated macrophages and their crosstalk with the tumor microenvironment.Cell discovery · 2026Article
- Predicting immunotherapy benefit in leiomyosarcoma through active chromatin cfDNA profiling.NPJ precision oncology · 2026Article
- Multifaceted roles of miR‑124 in cancer: Molecular mechanisms and clinical prospects (Review).International journal of oncology · 2026Review
- comBO: A combined human bone and lympho-myeloid bone marrow organoid for preclinical modeling of hematopoietic disorders.Cell stem cell · 2026Article
- Ablation of CD38 in multiple myeloma cells leads to an aggressive phenotype in a mouse xenograft model.Blood advances · 2026Article
- Multi-omics signatures of chronic inflammation across immune-related disease states.Frontiers in immunology · 2026Article
- Teclistamab for Relapsed or Refractory Multiple Myeloma: A Review of Efficacy, Safety, Resistance Mechanisms and Future Directions.Biologics : targets & therapy · 2026Review
- A single-cell atlas characterizes dysregulation of the bone marrow immune microenvironment associated with outcomes in multiple myeloma.Nature cancer · 2026Article
- From bone marrow to the tumor microenvironment: how neutrophil maturation shapes cancer immunity.Cancer biology & medicine · 2025Article
- A single-cell atlas reveals the tumorigenesis and microenvironment status of primary tracheobronchial tumors.NPJ precision oncology · 2025Article
- Single-Cell Immune Profiling Reveals Neutrophils Promote Myasthenia Gravis Exacerbation Through BAFF Secretion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Dynamic remodelling of epithelial plasticity in colorectal cancer from single-cell and spatially resolved perspectives.Journal of translational medicine · 2025Article
- Characterization of the bone marrow architecture of multiple myeloma using spatial transcriptomics.Communications biology · 2025Article
- Article
- Altered mesenchymal and endothelial subsets in interstitial bone marrow and focal lesions in myeloma patients and SCID-hu mice.Haematologica · 2025Article
Corrections and comments
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Authors and funding
20 authors.
Funding
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Abstract
Human bone marrow permanently harbors high numbers of neutrophils, and a tumor-supportive bias of these cells could significantly impact bone marrow-confined malignancies. In individuals with multiple myeloma, the bone marrow is characterized by inflammatory stromal cells with the potential to influence neutrophils. We investigated myeloma-associated alterations in human marrow neutrophils and the impact of stromal inflammation on neutrophil function. Mature neutrophils in myeloma marrow are activated and tumor supportive and transcribe increased levels of IL1B and myeloma cell survival factor TNFSF13B (BAFF). Interactions with inflammatory stromal cells induce neutrophil activation, including BAFF secretion, in a STAT3-dependent manner, and once activated, neutrophils gain the ability to reciprocally induce stromal activation. After first-line myeloid-depleting antimyeloma treatment, human bone marrow retains residual stromal inflammation, and newly formed neutrophils are reactivated. Combined, we identify a neutrophil-stromal cell feed-forward loop driving tumor-supportive inflammation that persists after treatment and warrants novel strategies to target both stromal and immune microenvironments in multiple myeloma.
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Registered trials
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