Evidence map›Paper›PMID 33675065›Full record

ReviewEuropean journal of immunology2021

Janus kinase signaling as risk factor and therapeutic target for severe SARS-CoV-2 infection.

Farzan Solimani, Katharina Meier, Kamran Ghoreschi

Open access · hybridAbstract readReview
In one paragraph

Review in European journal of immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 4 pooled it
2.2field-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

25 citing papers in PubMed, 4 syntheses or guidelines pooled it, 37 citations in OpenAlex.

  1. Large-scale meta-analysis of infection risk with JAK-STAT inhibitors in 29,000 patients.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026
    Pooled it
  2. Janus kinase inhibitors for the treatment of COVID-19.The Cochrane database of systematic reviews · 2022
    Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Article
  8. Article
  9. Unraveled role of TLR7-mediated interferon signaling activation in COVID-19.Frontiers in cellular and infection microbiology · 2025
    Review
  10. Review
  11. Article
  12. Host-Based Treatments for Severe COVID-19.Current issues in molecular biology · 2023
    Review
  13. Review
  14. Article
  15. Review
  16. Small molecules in the treatment of COVID-19.Signal transduction and targeted therapy · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Farzan SolimaniDepartment of Dermatology, Venereology and Allergology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Katharina MeierDepartment of Dermatology, Venereology and Allergology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Kamran GhoreschiDepartment of Dermatology, Venereology and Allergology, Charité-Universitätsmedizin Berlin, Berlin, Germany.ORCID 0000-0002-5526-7517
Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytokine signaling, especially interferon (IFN) signaling is closely linked to several aspects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. During initial SARS-CoV-2 infection, symptomatic patients present with impaired type I/III IFN-mediated antiviral responses. Interestingly, IFNs regulate the cellular entry receptor for SARS-CoV-2 on epithelial and endothelial cells. As reported recently, critically ill COVID-19 patients show genetic polymorphisms in one IFN receptor gene (IFNRA2) and in a gene locus near the Janus kinase (JAK) TYK2, which is key for IFN, interleukin (IL)-12 and IL-23 signaling, and T helper (Th) 1/Th17 cell-mediated antiviral immune responses. In the advanced stage of the disease, critically ill COVID-19 patients develop a cytokine storm where many inflammatory mediators using the JAK/STAT signaling pathway such as IL-6, IFN-γ, the granulocyte colony-stimulating factor (G-CSF) or IL-2, and chemokines result in an influx of macrophages and neutrophils damaging the lung tissue. The knowledge on the cytokine and JAK/STAT signaling pathways in severe COVID-19 disease explains the promising first results with JAK inhibitors like baricitinib, which not only dampen the inflammation but in the case of baricitinib also affect virus replication and endocytosis in target cells. Here, we summarize the current immunological associations of SARS-CoV-2 infection with cytokine signaling, the JAK/STAT pathway, and the current clinical stage of JAK inhibitors for improving severe COVID-19 disease.

Indexed as

COVID-19 Drug TreatmentAzetidinesCOVID-19Cytokine Release SyndromeCytokinesHumansInterferon LambdaInterferonsInterferon Type INitrilesPurinesPyrazolesPyrimidinesReceptors, InterferonSARS-CoV-2SulfonamidesAzetidinesbaricitinibCytokinesInterferon LambdaInterferonsInterferon Type INitrilesPurinesPyrazolesPyrimidinesReceptors, InterferonruxolitinibSulfonamidesTYK2 KinaseTYK2 protein, humancytokine stormJAK inhibitorsJanus kinaseSARS-CoV-2severe COVID-19

Identifiers

PMID33675065
PMCPMC8250126
OpenAlexW3135328714

What OpenQuestion 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 OpenQuestion graph.