Evidence map›Paper›PMID 31875268›Full record

ReviewCurrent topics in microbiology and immunology2023

Pyroptosis in Antiviral Immunity.

Teneema Kuriakose, Thirumala-Devi Kanneganti

Open access · greenAbstract readReview
In one paragraph

Review in Current topics in microbiology and immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Teneema KuriakoseDepartment of Immunology, St. Jude Children's Research Hospital, MS #351, 262 Danny Thomas Place, 38105-3678, Memphis, TN, USA.
Thirumala-Devi KannegantiDepartment of Immunology, St. Jude Children's Research Hospital, MS #351, 262 Danny Thomas Place, 38105-3678, Memphis, TN, USA. Thirumala-Devi.Kanneganti@STJUDE.ORG.
St. Jude Children's Research Hospital · US

Funding

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
NLR signaling in colitis and colorectal tumorigenesisR01CA163507 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2012 to 2020
$3.5M
Inflammatory Caspases in Innate Immunity and InflammationR01AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2012 to 2016
$2.2M
NCI NIH HHS R01 CA163507NIAID NIH HHS R01 AI101935NIAID NIH HHS R01 AI124346NIAID NIH HHS R37 AI101935NIAMS NIH HHS R01 AR056296
6 · The paper itself

Abstract

Pyroptosis is a form of lytic, programmed cell death that functions as an innate immune effector mechanism to facilitate host defense against pathogenic microorganisms, including viruses. This type of proinflammatory cell death is orchestrated by proteolytic activation of human or mouse caspase-1, mouse caspase-11 and human caspase-4 and caspase-5 in response to infectious and inflammatory stimuli. Induction of pyroptosis requires either a canonical inflammasome responsible for caspase-1 activation or a noncanonical complex composed of caspase-11 in mice or caspase-4 or caspase-5 in humans. Recent studies have identified the pore-forming protein gasdermin D, a substrate of these inflammatory caspases, as an executioner of pyroptosis. The membrane pores formed by gasdermin D facilitate release of proinflammatory cytokines IL-1β and IL-18 and consequent biologic effects of these cytokines together with other released components. Pyroptosis, like other forms of programmed cell death, helps eliminate infected cells and thereby restricts the replicative niche, undermining survival and proliferation of intracellular pathogens. This includes viruses as well as bacteria, where ample evidence supports a critical role for inflammasome effector functions and cell death in host defense. Viruses have evolved their own mechanisms to modulate inflammasome signaling and pyroptosis. Here, we review the current literature regarding the role of pyroptosis in antiviral immune responses.

Indexed as

InflammasomesPyroptosisAnimalsCaspasesCytokinesGasderminsHumansMiceCaspasesCytokinesGasderminsInflammasomesAIM2Caspase-1Caspase-11CaspasesCell deathGasderminInfectionInflammasomesInflammationInnate immunityNLRP3PANoptosisPyroptosisViruses

Identifiers

PMID31875268
PMCPMC7314647
OpenAlexW2998692163

What OpenQuestion holds

Textmetadata
LicenceTDM
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.