ReviewBiomedicines2025
Immunodynamic Disruption in Sepsis: Mechanisms and Strategies for Personalized Immunomodulation.
Review in Biomedicines, 2025. 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.
- Endothelial Collapse as a Convergent Immunovascular Phenotype in Sepsis and Severe Arboviral Disease: The SIMVAC Model.Pathogens (Basel, Switzerland) · 2026Review
- From Glycocalyx Shedding to Microvascular Collapse in Sepsis: Endothelial Pathophysiology, Organ Dysfunction, and Mechanistic Biomarkers.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- EBV reactivation and immunoparalysis indicate a harmful immune endotype in sepsis.Critical care (London, England) · 2026Article
- Decoding Immune Dysregulation in Sepsis Through Extracellular Vesicles: A Path to Precision Medicine.Pharmaceutics · 2026Review
- Regulated cell death in sepsis: reframing NETosis within the spectrum of apoptosis and inflammatory lytic death.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Immune Endotype-Guided Precision Immunotherapy in Sepsis: From Transcriptomics to Bedside Application.Cureus · 2026Review
- Article
- Extracellular Vesicle-Derived MicroRNAs' Value in Diagnosing and Predicting Clinical Outcomes in Patients with COVID-19 and Bacterial Sepsis.International journal of molecular sciences · 2026Article
- Peripheral Blood Mononuclear Cells in Sepsis: Immune Trajectories, Monocyte Dysfunction, and Translational Biomarkers.Journal of inflammation research · 2026Review
- The incremental value of a novel immuno-inflammatory index (SIICI) in predicting sepsis after ureteroscopic lithotripsy: development and validation of a nomogram.Frontiers in cellular and infection microbiology · 2026Article
- Mechanisms and therapeutics of immunometabolic reprogramming driving macrophage-ECs interactions in sepsis-associated ARDS from the gut-lung axis perspective.Frontiers in immunology · 2026Review
- Intracellular ATP Levels in CD4Journal of inflammation research · 2026Article
- Gut microbiota and sepsis: mechanisms, clinical correlations, and therapeutic prospects.Frontiers in medicine · 2026Article
- Levels of myeloid-derived suppressor cell-like cells in early sepsis: a comparative study with non-septic patients.Frontiers in immunology · 2026Observational
- Article
- Sepsis in multimorbidity: a domain-based framework for systemic vulnerability and precision care.Frontiers in medicine · 2026Review
- Combatting sepsis-induced myocardial dysfunction: emerging mechanisms and immunomodulatory breakthroughs.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is a life-threatening syndrome caused by a dysregulated host response to infection. It follows a dynamic course in which early hyperinflammation coexists and overlaps with progressive immune suppression, a process best described as immunodynamic disruption. Key mechanisms include extensive lymphocyte death, expansion of regulatory T cells, impaired antigen presentation, and persistent activation of inhibitory checkpoints such as programmed cell death protein 1 (PD-1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4). These changes reduce immune competence and increase vulnerability to secondary infections. Clinically, reduced expression of Human Leukocyte Antigen-DR (HLA-DR) on monocytes and persistent lymphopenia have emerged as robust biomarkers for patient stratification and timing of immunomodulatory therapies. Beyond the acute phase, many survivors do not achieve full immune recovery but instead develop a Persistent Immune Remnant, defined as long-lasting immune, metabolic, and endothelial dysfunction despite apparent clinical resolution. Recognizing PIR emphasizes the need for long-term monitoring and biomarker-guided interventions to restore immune balance. To integrate these observations, we propose the SIMMP-Sepsis model (Sepsis-Associated Persistent Multiorgan Immunometabolic Syndrome), which links molecular dysfunction to clinical trajectories and provides a framework for developing precision immunotherapies. This perspective reframes sepsis not only as an acute crisis but also as a chronic immunometabolic syndrome, where survival marks the beginning of active immune restoration.
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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.