Evidence map›Paper›PMID 35461172›Full record

ReviewCytokine2022

SARS-CoV-2 triggering autoimmune diseases.

Leila Mobasheri, Mohammad Hossein Nasirpour, Elham Masoumi, Afsaneh Foolady Azarnaminy, Mozhdeh Jafari, Seyed-Alireza Esmaeili

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cytokine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 3 pooled it
14.4field-weighted citation impact, top 1% 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

70 citing papers in PubMed, 3 syntheses or guidelines pooled it, 119 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Observational
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. NETosis: A key player in autoimmunity, COVID-19, and long COVID.Journal of translational autoimmunity · 2025
    Review
  17. Article
  18. Review
  19. Article
  20. Autoantibodies targeting angiotensin-converting enzyme 2 are prevalent and not induced by SARS-CoV-2 infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article

10 more citing papers are in PubMed but not listed here.

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 1 country.

Leila MobasheriDepartment of Pharmacology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Mohammad Hossein NasirpourDepartment of Medical Genetics, Institute of Medical Biotechnology, National Institute of Genetic Engineering and Biotechnology (NIGEB), Tehran, Iran.
Elham MasoumiDepartment of Immunology, School of Medicine, Ilam University of Medical Sciences, Ilam, Iran; Student Research Committee, School of Medicine, Ilam University of Medical Sciences, Ilam, Iran.
Afsaneh Foolady AzarnaminyDepartment of Anesthesiology, Social Security Organization Hospital, Ardabil, Iran.
Mozhdeh JafariImmunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Immunology Department, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Seyed-Alireza EsmaeiliImmunology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran; Immunology Department, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: Esmaeiliar@mums.ac.ir.
Mashhad University of Medical Sciences · IRMedical University of Ilam · IRNational Institute of Genetic Engineering and Biotechnology · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmunity, hyperstimulation of the immune system, can be caused by a variety of reasons. Viruses are thought to be important environmental elements that contribute to the development of autoimmune antibodies. It seems that viruses cause autoimmunity with mechanisms such as molecular mimicry, bystander activation of T cells, transient immunosuppression, and inflammation, which has also been seen in post-Covid-19 autoimmunity. Infection of respiratory epithelium by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) dysregulates the immune response, triggers both innate and acquired immunity that led to the immune system's hyperactivation, excessive cytokine secretion known as "cytokine storm," and finally acute respiratory distress syndrome (ARDS) associated with high mortality. Any factor in the body that triggers chronic inflammation can contribute to autoimmune disease, which has been documented during the Covid-19 pandemic. It has been observed that some patients produce autoantibody and autoreactive CD4

Indexed as

Autoimmune DiseasesCOVID-19Adaptive ImmunityAutoantibodiesCD8-Positive T-LymphocytesHumansInflammationPandemicsSARS-CoV-2AutoantibodiesAutoimmune diseaseAutoimmunityCovid-19CytokineSARS-CoV-2

Identifiers

PMID35461172
PMCPMC8979824
OpenAlexW4224307955

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.