ArticleCell proliferation2024
Apoptotic bodies inhibit inflammation by PDL1-PD1-mediated macrophage metabolic reprogramming.
Article in Cell proliferation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
17 citing papers in PubMed, 17 citations in OpenAlex.
- HO-1-modified umbilical cord MSCs alleviate pulmonary arterial hypertension by reducing inflammation and endothelial dysfunction.Stem cells translational medicine · 2026Article
- Extracellular vesicles in colorectal cancer: immunomodulation, diagnostics, and therapeutic perspectives.Medical oncology (Northwood, London, England) · 2026Review
- Macrophage metabolic reprogramming in sepsis-associated acute lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2026Review
- Tissue regeneration strategies based on mesenchymal stem cell-derived extracellular vesicles: from bench to bedside.Burns & trauma · 2026Review
- Targeting macrophage polarization: mechanisms and potential of mesenchymal stromal/stem cells therapy in acne treatment- a narrative review.Frontiers in immunology · 2026Review
- Preoperative systemic inflammation and muscle fatty infiltration are prognostic factors for quadriceps atrophy following anterior cruciate ligament reconstruction.Frontiers in immunology · 2026Article
- Temporal dynamics of macrophage activation duringVirulence · 2025Article
- Mesenchymal stem cells for lung diseases: focus on immunomodulatory action.Cell death discovery · 2025Review
- Native and Engineered Extracellular Vesicles for the Treatment of Acute Lung Injury and Acute Respiratory Distress Syndrome.Small science · 2025Article
- M2-ApoBDs as a therapeutic strategy for systemic lupus erythematosus: targeted macrophage reprogramming and treg differentiation.Journal of nanobiotechnology · 2025Article
- Apoptotic mesenchymal stem cells and their secreted apoptotic extracellular vesicles: therapeutic applications and mechanisms.Stem cell research & therapy · 2025Review
- Macrophage‑driven pathogenesis in acute lung injury/acute respiratory disease syndrome: Harnessing natural products for therapeutic interventions (Review).Molecular medicine reports · 2025Review
- Unlocking the secrets of glucose metabolism reprogramming: the role in pulmonary diseases.Frontiers in pharmacology · 2025Review
- Harmonising cellular conversations: decoding the vital roles of extracellular vesicles in respiratory system intercellular communications.European respiratory review : an official journal of the European Respiratory Society · 2024Review
- Apoptotic Vesicles Modulate Endothelial Metabolism and Ameliorate Ischemic Retinopathy via PD1/PDL1 Axis.Advanced healthcare materials · 2024Article
- Article
- Apoptotic bodies inhibit inflammation by PDL1-PD1-mediated macrophage metabolic reprogramming.Cell proliferation · 2024Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Apoptosis triggers immunoregulation to prevent and suppress inflammation and autoimmunity. However, the mechanism by which apoptotic cells modulate immune responses remains largely elusive. In the context of allogeneic mesenchymal stem cells (MSCs) transplantation, long-term immunoregulation is observed in the host despite the short survive of the injected MSCs. In this study, utilizing a mouse model of acute lung injury (ALI), we demonstrate that apoptotic bodies (ABs) released by transplanted human umbilical cord MSCs (UC-MSCs) convert the macrophages from a pro-inflammatory to an anti-inflammatory state, thereby ameliorating the disease. Mechanistically, we identify the expression of programmed cell death 1 ligand 1 (PDL1) on the membrane of UC-MSCs-derived ABs, which interacts with programmed cell death protein 1 (PD1) on host macrophages. This interaction leads to the reprogramming of macrophage metabolism, shifting from glycolysis to mitochondrial oxidative phosphorylation via the Erk-dependent pathway in ALI. Importantly, we have reproduced the PDL1-PD1 effects of ABs on metabolic switch using alveolar macrophages from patients with ALI, suggesting the potential clinical implications of developing therapeutic strategies for the patients.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.