ArticleCells2020
Disharmonic Inflammatory Signatures in COVID-19: Augmented Neutrophils' but Impaired Monocytes' and Dendritic Cells' Responsiveness.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
90 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.
- Pooled it
- Differential regulation of neutrophil degranulation by p38 MAPK and mitochondrial ROS duringFrontiers in pharmacology · 2026Article
- Age influences blood cell-based immune deregulation antibody response and unfavorable clinical outcomes in COVID-19 patients.Scientific reports · 2025Article
- Evaluation of Dendritic Cell Subpopulations Frequency in COVID-19 Patients and their Correlation with Disease Severity.Iranian journal of immunology : IJI · 2025Article
- Comparative analysis of neutrophil dynamics and disease in SARS-CoV-2 Delta and Omicron variants utilizing anFrontiers in immunology · 2025Article
- Emergence of dysfunctional neutrophils with a defect in arginase-1 release in severe COVID-19.JCI insight · 2024Article
- The Dysregulation of the Monocyte-Dendritic Cell Interplay Is Associated with In-Hospital Mortality in COVID-19 Pneumonia.Journal of clinical medicine · 2024Article
- A Review on Role of Inflammation in Coronavirus Disease.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Evidence of autoinflammation as a principal mechanism of myocardial injury in SARS-CoV-2 PCR-positive medical examiner cases.Diagnostic pathology · 2023Article
- Preliminary Comparison of Molecular Antioxidant and Inflammatory Mechanisms Determined in the Peripheral Blood Granulocytes of COVID-19 Patients.International journal of molecular sciences · 2023Article
- Obesity in Severe COVID-19 Patients Has a Distinct Innate Immune Phenotype.Biomedicines · 2023Article
- Purinergic signaling pathway in severe COVID-19.Current opinion in pharmacology · 2023Review
- Article
- Neutrophil Extracellular Traps in Airway Diseases: Pathological Roles and Therapeutic Implications.International journal of molecular sciences · 2023Review
- Neutrophil autophagy and NETosis in COVID-19: perspectives.Autophagy · 2023Review
- The Effects of Statins on Respiratory Symptoms and Pulmonary Fibrosis in COVID-19 Patients with Diabetes Mellitus: A Longitudinal Multicenter Study.Archivum immunologiae et therapiae experimentalis · 2023Article
- From Co-Infections to Autoimmune Disease via Hyperactivated Innate Immunity: COVID-19 Autoimmune Coagulopathies, Autoimmune Myocarditis and Multisystem Inflammatory Syndrome in Children.International journal of molecular sciences · 2023Review
- Lipid alternations in the plasma of COVID-19 patients with various clinical presentations.Frontiers in immunology · 2023Article
- High-dimensional comparison of monocytes and T cells in post-COVID and idiopathic pulmonary fibrosis.Frontiers in immunology · 2023Article
- Initial immune response after exposure toFrontiers in immunology · 2023Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
COVID-19, caused by SARS-CoV-2 virus, emerged as a pandemic disease posing a severe threat to global health. To date, sporadic studies have demonstrated that innate immune mechanisms, specifically neutrophilia, NETosis, and neutrophil-associated cytokine responses, are involved in COVID-19 pathogenesis; however, our understanding of the exact nature of this aspect of host-pathogen interaction is limited. Here, we present a detailed dissection of the features and functional profiles of neutrophils, dendritic cells, and monocytes in COVID-19. We portray the crucial role of neutrophils as drivers of hyperinflammation associated with COVID-19 disease via the shift towards their immature forms, enhanced degranulation, cytokine production, and augmented interferon responses. We demonstrate the impaired functionality of COVID-19 dendritic cells and monocytes, particularly their low expression of maturation markers, increased PD-L1 levels, and their inability to upregulate phenotype upon stimulation. In summary, our work highlights important data that prompt further research, as therapeutic targeting of neutrophils and their associated products may hold the potential to reduce the severity of COVID-19.
Indexed as
Identifiers
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.