ArticleBlood2009
Impaired apoptotic cell clearance in CGD due to altered macrophage programming is reversed by phosphatidylserine-dependent production of IL-4.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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.
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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
82 citing papers in PubMed, 126 citations in OpenAlex.
- High Levels of IL-18 and IFN-γ in Chronically Inflamed Tissue in Chronic Granulomatous Disease.Frontiers in immunology · 2019Trial
- The role of myeloid immune cells in lung epithelial repair.American journal of physiology. Lung cellular and molecular physiology · 2026Review
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- Roles of efferocytosis in wound repair: Process, cells, and signals.Genes & diseases · 2026Review
- The type 1 and type 3 immune responses underlying the tissue inflammation associated with NOX2 deficiency.Frontiers in immunology · 2026Review
- Neutrophil death pathways in myocardial infarction: the balance between injury and repair.Frontiers in immunology · 2026Review
- Efferocytosis in tissue engineering: A comprehensive review of emerging therapeutic strategies for enhanced tissue repair and regeneration.Bioactive materials · 2025Review
- The trapping of live neutrophils by macrophages during infection.Cell death & disease · 2025Article
- A LTBiScience · 2024Article
- Inflammatory Complications in Chronic Granulomatous Disease.Journal of clinical medicine · 2024Review
- TNFα: TNFR1 signaling inhibits maturation and maintains the pro-inflammatory programming of monocyte-derived macrophages in murine chronic granulomatous disease.Frontiers in immunology · 2024Article
- Enhancement of Anti-inflammatory Effects of Synthetic High-Density Lipoproteins by Incorporation of Anionic Lipids.Molecular pharmaceutics · 2023Article
- Anti-Inflammatory Neutrophil Functions in the Resolution of Inflammation and Tissue Repair.Cells · 2022Review
- Meta-Analysis and Systematic Review of the Association between a HypoactiveAntioxidants (Basel, Switzerland) · 2022Review
- Crosstalk between Heme Oxygenase-1 and Iron Metabolism in Macrophages: Implications for the Modulation of Inflammation and Immunity.Antioxidants (Basel, Switzerland) · 2022Review
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- Environment tames CGD macrophages.Blood · 2022Article
- Neutrophil-Derived Tumor Necrosis Factor Drives Fungal Acute Lung Injury in Chronic Granulomatous Disease.The Journal of infectious diseases · 2021Article
- STAT6 Signaling Mediates PPARγ Activation and Resolution of Acute Sterile Inflammation in Mice.Cells · 2021Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic granulomatous disease (CGD) is characterized by overexuberant inflammation and autoimmunity that are attributed to deficient anti-inflammatory signaling. Although regulation of these processes is complex, phosphatidylserine (PS)-dependent recognition and removal of apoptotic cells (efferocytosis) by phagocytes are potently anti-inflammatory. Since macrophage phenotype also plays a beneficial role in resolution of inflammation, we hypothesized that impaired efferocytosis in CGD due to macrophage skewing contributes to enhanced inflammation. Here we demonstrate that efferocytosis by macrophages from CGD (gp91(phox)(-/-)) mice was suppressed ex vivo and in vivo. Alternative activation with interleukin 4 (IL-4) normalized CGD macrophage efferocytosis, whereas classical activation by lipopolysaccharide (LPS) plus interferon gamma (IFNgamma) had no effect. Importantly, neutralization of IL-4 in wild-type macrophages reduced macrophage efferocytosis, demonstrating a central role for IL-4. This effect was shown to involve 12/15 lipoxygenase and activation of peroxisome-proliferator activated receptor gamma (PPARgamma). Finally, injection of PS (whose exposure is lacking on CGD apoptotic neutrophils) in vivo restored IL-4-dependent macrophage reprogramming and efferocytosis via a similar mechanism. Taken together, these findings support the hypothesis that impaired PS exposure on dying cells results in defective macrophage programming, with consequent efferocytic impairment and has important implications in understanding the underlying cause of enhanced inflammation in CGD.
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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.