Evidence map›Paper›PMID 34512643›Full record

ReviewFrontiers in immunology2021

COVID-19 Immunobiology: Lessons Learned, New Questions Arise.

Aimilios Kaklamanos, Konstantinos Belogiannis, Panagiotis Skendros, Vassilis G Gorgoulis, Panayiotis G Vlachoyiannopoulos, Athanasios G Tzioufas

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 10% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  9. COVID-19 and cellular senescence.Nature reviews. Immunology · 2023
    Review
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  12. Review
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  14. Review
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  17. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Aimilios KaklamanosDepartment of Pathophysiology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Konstantinos BelogiannisMolecular Carcinogenesis Group, Department of Histology and Embryology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Panagiotis SkendrosFirst Department of Internal Medicine and Laboratory of Molecular Hematology, University Hospital of Alexandroupolis, Democritus University of Thrace, Alexandroupolis, Greece.
Vassilis G GorgoulisMolecular Carcinogenesis Group, Department of Histology and Embryology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Panayiotis G VlachoyiannopoulosDepartment of Pathophysiology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Athanasios G TzioufasDepartment of Pathophysiology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
National and Kapodistrian University of Athens · GRBiomedical Research Foundation of the Academy of Athens · GRDemocritus University of Thrace · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is strong evidence that COVID-19 pathophysiology is mainly driven by a spatiotemporal immune deregulation. Both its phenotypic heterogeneity, spanning from asymptomatic to severe disease/death, and its associated mortality, are dictated by and linked to maladaptive innate and adaptive immune responses against SARS-CoV-2, the etiologic factor of the disease. Deregulated interferon and cytokine responses, with the contribution of immune and cellular stress-response mediators (like cellular senescence or uncontrolled inflammatory cell death), result in innate and adaptive immune system malfunction, endothelial activation and inflammation (endothelitis), as well as immunothrombosis (with enhanced platelet activation, NET production/release and complement hyper-activation). All these factors play key roles in the development of severe COVID-19. Interestingly, another consequence of this immune deregulation, is the production of autoantibodies and the subsequent development of autoimmune phenomena observed in some COVID-19 patients with severe disease. These new aspects of the disease that are now emerging (like autoimmunity and cellular senescence), could offer us new opportunities in the field of disease prevention and treatment. Simultaneously, lessons already learned from the immunobiology of COVID-19 could offer new insights, not only for this disease, but also for a variety of chronic inflammatory responses observed in autoimmune and (auto)inflammatory diseases.

Indexed as

COVID-19HumansSARS-CoV-2autoimmunityCOVID-19endothelitisimmune deregulationimmunothrombosisSARS-CoV-2senescence

Identifiers

PMID34512643
PMCPMC8427766
OpenAlexW3198552032

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.