ReviewBiology2023
Exploring the Role of Immune System and Inflammatory Cytokines in SARS-CoV-2 Induced Lung Disease: A Narrative Review.
Review in Biology, 2023. 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
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
17 citing papers in PubMed, 32 citations in OpenAlex.
- Autoantibodies neutralizing type I interferons in COVID-19 patients from southern Brazil.Journal of human immunity · 2026Article
- Immune cell interactions and lung damage in SARS-CoV-2 special attention on monocytes/macrophages, T and B lymphocytes, dendritic cells and Toll-like receptors in SARS-CoV-2.American journal of clinical and experimental immunology · 2026Review
- Revisiting the monocrotaline-treated rat as a model of inflammatory lung disease: COVID-19 and future pandemic threats?Animal models and experimental medicine · 2025Review
- Frequency of IgE antibody response to SARS-CoV-2 RBD protein across different disease severity COVID19 groups.Virology journal · 2025Article
- Circulating Endothelin 1 but Not Transforming Growth Factor-β Levels Are Reduced after Pulmonary Endarterectomy in Subjects Affected by Chronic Thromboembolic Pulmonary Hypertension: A Prospective Cohort Study.Journal of clinical medicine · 2024Article
- Article
- Observational
- Cutaneous Leishmaniasis Hampers COVID-19: A Controlled Cross-Sectional Study in High-Burden Endemic Areas of Iran.Journal of epidemiology and global health · 2024Article
- SARS-CoV-2: A Glance at the Innate Immune Response Elicited by Infection and Vaccination.Antibodies (Basel, Switzerland) · 2024Review
- COVID-19 influenced gut dysbiosis, post-acute sequelae, immune regulation, and therapeutic regimens.Frontiers in cellular and infection microbiology · 2024Review
- Effectiveness of Drug Repurposing and Natural Products Against SARS-CoV-2: A Comprehensive Review.Clinical pharmacology : advances and applications · 2024Review
- Article
- COVID-19 Complications: Oxidative Stress, Inflammation, and Mitochondrial and Endothelial Dysfunction.International journal of molecular sciences · 2023Review
- Sustained Treatment Response after Intravenous Cyclophosphamide in a Patient with Therapy-Resistant COVID-19 Acute Respiratory Distress Syndrome: A Case Report.Journal of clinical medicine · 2023Article
- Assessing Humoral Immuno-Inflammatory Pathways Associated with Respiratory Failure in COVID-19 Patients.Journal of clinical medicine · 2023Article
- Predictors of ICU Admission in Children with COVID-19: Analysis of a Large Mexican Population Dataset.Journal of clinical medicine · 2023Article
- Comparative analysis of clinical and immunological profiles across Omicron BA.5.2 subvariants using next-generation sequencing in a Chinese cohort.Frontiers in cellular and infection microbiology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative pathogen of coronavirus disease 19 (COVID-19). COVID-19 can manifest with a heterogenous spectrum of disease severity, from mild upper airways infection to severe interstitial pneumonia and devastating acute respiratory distress syndrome (ARDS). SARS-CoV-2 infection may induce an over activation of the immune system and the release of high concentrations of pro-inflammatory cytokines, leading to a "cytokine storm", a recognized pathogenetic mechanism in the genesis of SARS-CoV-2-induced lung disease. This overproduction of inflammatory cytokines has been recognized as a poor prognostic factor, since it can lead to disease progression, organ failure, ARDS and death. Moreover, the immune system shows dysregulated activity, particularly through activated macrophages and T-helper cells and in the co-occurrent exhaustion of lymphocytes. We carried out a non-systematic literature review aimed at providing an overview of the current knowledge on the pathologic mechanisms played by the immune system and the inflammation in the genesis of SARS-CoV-2-induced lung disease. An overview on potential treatments for this harmful condition and for contrasting the "cytokine storm" has also been presented. Finally, a look at the experimented experimental vaccines against SARS-CoV-2 has been included.
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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.