ReviewFrontiers in immunology2022
The "Self-Sacrifice" of ImmuneCells in Sepsis.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Pooled it
- Heparanase inhibition leads to improvement in patients with acute gastrointestinal injuries induced by sepsis.World journal of gastroenterology · 2023Trial
- Early prediction of sepsis in the ICU: a comparative analysis of multiple machine-learning algorithms using the MIMIC-III database.BMC medical informatics and decision making · 2026Article
- The metabolite α-ketoglutarate induces AIM2-dependent PANoptosis through demethylase TET2.Cell communication and signaling : CCS · 2026Article
- A Histone Deacetylase Activity Model for the Discovery and Validation of Sepsis Biomarkers.Endocrine, metabolic & immune disorders drug targets · 2026Article
- Lymphocyte function inhibition and exhaustion in sepsis: mechanisms and applications.Frontiers in immunology · 2026Review
- PCSK9 Promotes Platelet Activation and NET Formation, Aggravating Pulmonary Microthrombosis in Sepsis-Induced Lung Injury.Biomedicines · 2025Article
- O‑GlcNAcylation: The crosstalk between infection immunity and autophagy in sepsis (Review).Molecular medicine reports · 2025Review
- NETosis and pyroptosis of immune cells in sepsis.Journal of translational internal medicine · 2025Article
- SPI1 upregulated LILRB2 to enhance the immunosuppressive phenotype of LPS-tolerant macrophages by inhibiting TLR8-mediated MyD88/NF-κB signaling.Biology direct · 2025Article
- Neutrophil Extracellular Traps in Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis: Diagnostic and Clinical Significance-A Review of the Current Literature.Journal of clinical medicine · 2025Review
- Identification and validation of autophagy-related genes in sepsis based on bioinformatics studies.Virology journal · 2025Article
- BMAL1 deficiency in macrophages exacerbates sepsis-induced inflammatory response and organ damage by regulating PGC-1α.American journal of clinical and experimental immunology · 2025Article
- IL-10 to lymphocyte ratio (ILR) and lactate in the prognosis prediction and risk stratification of sepsis: a pilot study.Frontiers in medicine · 2025Article
- The Mechanisms of Sepsis Induced Coagulation Dysfunction and Its Treatment.Journal of inflammation research · 2025Review
- The Crucial Roles of Platelets as Immune Mediators in Sepsis.Journal of inflammation research · 2025Review
- Autophagy and autophagic cell death in sepsis: friend or foe?Journal of intensive care · 2024Review
- Caspase-8 in inflammatory diseases: a potential therapeutic target.Cellular & molecular biology letters · 2024Review
- Neutrophil Depletion Changes the N-Glycosylation Pattern of IgG in Experimental Murine Sepsis.International journal of molecular sciences · 2024Article
- The potential immunological mechanisms of sepsis.Frontiers in immunology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a life-threatening organ dysfunction caused by the host's malfunctioning response to infection. Due to its high mortality rate and medical cost, sepsis remains one of the world's most intractable diseases. In the early stage of sepsis, the over-activated immune system and a cascade of inflammation are usually accompanied by immunosuppression. The core pathogenesis of sepsis is the maladjustment of the host's innate and adaptive immune response. Many immune cells are involved in this process, including neutrophils, mononuclear/macrophages and lymphocytes. The immune cells recognize pathogens, devour pathogens and release cytokines to recruit or activate other cells in direct or indirect manner. Pyroptosis, immune cell-extracellular traps formation and autophagy are several novel forms of cell death that are different from apoptosis, which play essential roles in the progress of sepsis. Immune cells can initiate "self-sacrifice" through the above three forms of cell death to protect or kill pathogens. However, the exact roles and mechanisms of the self-sacrifice in the immune cells in sepsis are not fully elucidated. This paper mainly analyzes the self-sacrifice of several representative immune cells in the forms of pyroptosis, immune cell-extracellular traps formation and autophagy to reveal the specific roles they play in the occurrence and progression of sepsis, also to provide inspiration and references for further investigation of the roles and mechanisms of self-sacrifice of immune cells in the sepsis in the future, meanwhile, through this work, we hope to bring inspiration to clinical work.
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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.