ArticleCell death & disease2021
Immune complex-induced apoptosis and concurrent immune complex clearance are anti-inflammatory neutrophil functions.
Article in Cell death & disease, 2021. 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Alteration of the Gut-Lung Axis After Severe COVID-19 Infection and Modulation Through Probiotics: A Randomized, Controlled Pilot Study.Nutrients · 2024Trial
- Non-destructive debridement and tuneable ion release via magnesium abrasion and electro-dissolution promote bone regeneration and osseointegration of infected implants.Materials today. Bio · 2026Article
- Vitexin induces apoptosis and enhances daunorubicin efficacy in acute leukemia via modulation of the HIF-1α/Bcl-2/caspase-3 pathway.Scientific reports · 2025Article
- Interplay between survival and regulated cell death mechanisms during periodontitis progression: a systematic review.The Japanese dental science review · 2025Review
- Immunosenescence in Sepsis: Molecular Mechanisms and Potential Therapeutic Targets.Aging and disease · 2025Review
- Neutrophils in Rheumatoid Arthritis Synovium: Implications on Disease Activity and Inflammation State.Journal of inflammation research · 2025Article
- Bioscaffold materials resist infection and promote bone defect repair by regulating neutrophil function.Frontiers in bioengineering and biotechnology · 2025Review
- Neutrophils as key drivers of pulmonary fibrosis: unveiling mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Bioactive peptides and proteins for tissue repair: microenvironment modulation, rational delivery, and clinical potential.Military Medical Research · 2024Review
- Regulation of neutrophil associated RNASET2 expression in rheumatoid arthritis.Scientific reports · 2024Article
- The intricate relationship between autoimmunity disease and neutrophils death patterns: a love-hate story.Apoptosis : an international journal on programmed cell death · 2023Review
- Different types of cell death and their shift in shaping disease.Cell death discovery · 2023Review
- Release of immunomodulatory peptides at bacterial membrane interfaces as a novel strategy to fight microorganisms.The Journal of biological chemistry · 2023Article
- Anti-Inflammatory Neutrophil Functions in the Resolution of Inflammation and Tissue Repair.Cells · 2022Review
- Nanotechnology for Enhanced Cytoplasmic and Organelle Delivery of Bioactive Molecules to Immune Cells.Pharmaceutical research · 2022Review
- Functional significance of ion channels during macropinosome resolution in immune cells.Frontiers in physiology · 2022Review
- Crosstalk between B cells and neutrophils in rheumatoid arthritis.Immunology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Persistent neutrophilic inflammation drives host damage in autoimmune diseases that are characterized by abundant immune complexes. Insoluble immune complexes (iICs) potently activate pro-inflammatory neutrophil effector functions. We and others have shown that iICs also promote resolution of inflammation via stimulation of neutrophil apoptosis. We demonstrate here that iICs trigger FcγRIIa-dependent neutrophil macropinocytosis, leading to the rapid uptake, and subsequent degradation of iICs. We provide evidence that concurrent iIC-induced neutrophil apoptosis is distinct from phagocytosis-induced cell death. First, uptake of iICs occurs by FcγRII-stimulated macropinocytosis, rather than phagocytosis. Second, production of reactive oxygen species, but not iIC-internalization is a pre-requisite for iIC-induced neutrophil apoptosis. Our findings identify a previously unknown mechanism by which neutrophils can remove pro-inflammatory iICs from the circulation. Together iIC clearance and iIC-induced neutrophil apoptosis may act to prevent the potential escalation of neutrophilic inflammation in response to iICs.
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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.