Evidence map›Paper›PMID 31473100›Full record

ReviewImmunity2019

Inflammasomes: Threat-Assessment Organelles of the Innate Immune System.

Charles L Evavold, Jonathan C Kagan

Open access · bronzeAbstract readReview
In one paragraph

Review in Immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 1 pooled it
8.9field-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

99 citing papers in PubMed, 1 synthesis or guideline pooled it, 158 citations in OpenAlex.

  1. Pooled it
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  20. Novel cortisol trajectory sub-phenotypes in sepsis.Critical care (London, England) · 2024
    Article

39 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 2 institutions in 1 country.

Charles L EvavoldDivision of Gastroenterology, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA; Program in Immunology, Harvard Medical School, Boston, MA 02115, USA.
Jonathan C KaganDivision of Gastroenterology, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA; Program in Immunology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: jonathan.kagan@childrens.harvard.edu.
Boston Children's Hospital · USHarvard University · US

Funding

STRUCTURE-FUNCTION RELATIONSHIPS IN THE ALIMENTARY TRACTP30DK034854 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI JONATHAN C KAGAN · 1986 to 2026
$32.4M
Project 2: Genes required for dendritic cell responses to pathogens and T cellsU19AI133524 · NIAID · HARVARD MEDICAL SCHOOL · PI SHARPE, ARLENE H. · 2017 to 2021
$12.3M
Initiation and Regulation of Antiviral Innate ImmunityR01AI093589 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI KAGAN, JONATHAN C · 2011 to 2020
$4.4M
Defining the pathways activated by Toll-like Receptors to stimulate immunityR37AI116550 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI JONATHAN C KAGAN · 2021 to 2026
$3.3M
Characterization of the myddosome, a protein complex that controls TLR signalingR01AI116550 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI KAGAN, JONATHAN C · 2017 to 2020
$1.8M
Initiation and Regulation of Antiviral Innate ImmunityR56AI093589 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI KAGAN, JONATHAN C · 2021 to 2021
$531k
Disentangling the Death Decision: How Living Cells Release Interleukin-1F31AI138369 · NIAID · HARVARD MEDICAL SCHOOL · PI EVAVOLD, CHARLES LEE · 2019 to 2020
$66k
NIAID NIH HHS F31 AI138369NIAID NIH HHS R01 AI093589NIAID NIH HHS R01 AI116550NIAID NIH HHS R37 AI116550NIAID NIH HHS R56 AI093589NIAID NIH HHS U19 AI133524NIDDK NIH HHS P30 DK034854
6 · The paper itself

Abstract

Inflammasomes are supramolecular organizing centers that operate to drive interleukin-1 (IL-1)-dependent inflammation. Depending on context, inflammatory caspases act upstream or downstream of inflammasome assembly, serving as the principal enzymes that control activities of these organelles. In this review, we discuss mechanisms of inflammasome assembly and signaling. We posit that upstream regulatory proteins, classically known as pattern-recognition receptors, operate to assess infectious and non-infectious threats to the host. Threat assessment is achieved through two general strategies: (1) direct binding of receptors to microbial or host-derived ligands or (2) indirect detection of changes in cellular homeostasis. Upon activation, these upstream regulatory factors seed the assembly of inflammasomes, leading to IL-1 family cytokine release from living (hyperactive) or dead (pyroptotic) cells. The molecular and physiological consequences of these distinct cell fate decisions are discussed.

Indexed as

AnimalsCaspasesHumansImmune SystemImmunity, InnateInflammasomesInterleukin-1Multiprotein ComplexesReceptors, Pattern RecognitionSignal TransductionCaspasesInflammasomesInterleukin-1Multiprotein ComplexesReceptors, Pattern Recognition

Identifiers

PMID31473100
PMCPMC6801093
OpenAlexW2971280057

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.