ArticleNature communications2025
Defective neutrophil-derived exosomes facilitate macrophage activation through miR-122-5p in Behçet's disease.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- SCAP-Exo-Integrated CA/HACC Hydrogel Promotes Diabetic Wound Repair via miR-122-Driven Macrophage Phenotypic Transition.Advanced healthcare materials · 2026Article
- Advances in understanding exosome-mediated regulation of macrophage function.Frontiers in immunology · 2026Review
- Elucidating the Role of Neutrophils in the Inflammatory Response to Behcet Syndrome.Journal of inflammation research · 2026Review
- Macrophage-derived exosomes in autoimmune diseases: mechanistic insights and therapeutic implications.Immunologic research · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Behçet's disease (BD) is a life-threatening systemic vasculitis characterized by polymorphonuclear neutrophils (PMN) and macrophage activation. However, the interaction of PMN and macrophages remains elusive. To elucidate the potential dysregulation of BD PMN exosomes on macrophage activation, PMN exosomes from both BD patients and healthy controls are isolated, quantified and incubated with macrophages. We find that BD PMN exosomes are decreased and negatively correlated with C-reactive protein (CRP). PMN exosomes can suppress IL-6, TNF, CD80 and CD86 expressions on macrophages, which are attenuated in BD PMN exosomes. In addition, by miRNA sequencing of PMN exosomes, RNA sequencing of miRNA-transfected macrophages, and dual luciferase reporter assay validation of the miRNA target, we find that miR-122-5p is decreased in BD PMN exosomes, targeting IRF5, suppressing TLR4 signaling and IFN-β autocrine, eventually downregulating macrophage activation. Our study illustrates that BD PMN exosomes are decreased in both quantity and miR-122-5p, which impairs the potential immunoregulatory effects on macrophages through degrading IRF5 and suppressing IFN-β autocrine, shedding light on the interaction mechanism between PMN and macrophages.
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Registered trials
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