Evidence map›Paper›PMID 36419185›Full record

ReviewJournal of translational medicine2022

Innate immunity, cytokine storm, and inflammatory cell death in COVID-19.

Rajendra Karki, Thirumala-Devi Kanneganti

Open access · goldAbstract readReview
In one paragraph

Review in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 1 pooled it
10.9field-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

81 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Cytokine Storm Induction Linked to Multi-Organ Failure in Fatal Jellyfish Stings.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. HCK regulates NLRP12-mediated PANoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  20. Review

21 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

2 authors at 1 institution in 1 country.

Rajendra KarkiDepartment of Immunology, St. Jude Children's Research Hospital, MS #351, 262 Danny Thomas Place, Memphis, TN, 38105-3678, USA.
Thirumala-Devi KannegantiDepartment of Immunology, St. Jude Children's Research Hospital, MS #351, 262 Danny Thomas Place, Memphis, TN, 38105-3678, USA. Thirumala-Devi.Kanneganti@StJude.org.ORCID 0000-0002-6395-6443
St. Jude Children's Research Hospital · US

Funding

Innate immune sensors, inflammasomes, and inflammasome-mediated processes in cancerR35CA253095 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2020 to 2026
$7.0M
Role of NLR Inflammasomes in Autoinflammatory Diseases and Host DefenseR01AR056296 · NIAMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2008 to 2022
$5.9M
The Non-Inflammasome NLRs in Immunity and Host defenseR01AI124346 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2016 to 2026
$5.8M
Inflammatory Caspases in Innate Immunity and InflammationR37AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2017 to 2026
$4.9M
Targeting innate immune pathways, and inflammatory cell death in cytokine-mediated diseasesR01AI160179 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2021 to 2025
$4.2M
NCI NIH HHS CA253095NCI NIH HHS R35 CA253095NIAID NIH HHS AI101935NIAID NIH HHS AI124346NIAID NIH HHS AI160179NIAID NIH HHS R01 AI124346NIAID NIH HHS R01 AI160179NIAID NIH HHS R37 AI101935NIAMS NIH HHS AR056296NIAMS NIH HHS R01 AR056296
6 · The paper itself

Abstract

The innate immune system serves as the first line of defense against invading pathogens; however, dysregulated innate immune responses can induce aberrant inflammation that is detrimental to the host. Therefore, careful innate immune regulation is critical during infections. The coronavirus disease 2019 (COVID-19) pandemic is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has resulted in global morbidity and mortality as well as socio-economic stresses. Innate immune sensing of SARS-CoV-2 by multiple host cell pattern recognition receptors leads to the production of various pro-inflammatory cytokines and the induction of inflammatory cell death. These processes can contribute to cytokine storm, tissue damage, and acute respiratory distress syndrome. Here, we discuss the sensing of SARS-CoV-2 to induce innate immune activation and the contribution of this innate immune signaling in the development and severity of COVID-19. In addition, we provide a conceptual framework for innate immunity driving cytokine storm and organ damage in patients with severe COVID-19. A better understanding of the molecular mechanisms regulated by innate immunity is needed for the development of targeted modalities that can improve patient outcomes by mitigating severe disease.

Indexed as

COVID-19Cytokine Release SyndromeCell DeathHumansImmunity, InnateSARS-CoV-2IFNNecroptosisPANoptosisPANoptosomePyroptosisTNF

Identifiers

PMID36419185
PMCPMC9682745
OpenAlexW4309699937

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.