Evidence map›Paper›PMID 27524110›Full record

ArticleCellular & molecular immunology2017

The AIM2 inflammasome is a central regulator of intestinal homeostasis through the IL-18/IL-22/STAT3 pathway.

Rojo A Ratsimandresy, Mohanalaxmi Indramohan, Andrea Dorfleutner, Christian Stehlik

Open access · hybridAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 1 pooled it
9.4field-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

106 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.

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46 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

4 authors at 2 institutions in 1 country.

Rojo A RatsimandresyDivision of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Mohanalaxmi IndramohanDivision of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Andrea DorfleutnerDivision of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Christian StehlikDivision of Rheumatology, Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Northwestern University · USRobert H. Lurie Comprehensive Cancer Center of Northwestern University

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
Regulation of cytosolic pattern recognition receptor signaling in macrophagesR01AI099009 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI STEHLIK, CHRISTIAN · 2013 to 2022
$4.7M
Molecular Regulation of Systemic InflammationR01AI120625 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DORFLEUTNER, ANDREA, STEHLIK, CHRISTIAN · 2016 to 2020
$2.0M
Inflammasome Adaptor and Effectors in Cryopyrinopathies and Crystal ArthropathiesK01AR066739 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DORFLEUTNER, ANDREA · 2015 to 2019
$471k
A novel mouse model to monitor inflammasome activation in vivoR21AI120618 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI DORFLEUTNER, ANDREA, STEHLIK, CHRISTIAN · 2015 to 2016
$425k
NCI NIH HHS P30 CA060553NIAID NIH HHS R01 AI099009NIAID NIH HHS R01 AI120625NIAID NIH HHS R21 AI120618NIAMS NIH HHS K01 AR066739
6 · The paper itself

Abstract

Inflammasomes are important for maintaining intestinal homeostasis, and dysbiosis contributes to the pathology of inflammatory bowel disease (IBD) and increases the risk for colorectal cancer. Inflammasome defects contribute to chronic intestinal inflammation and increase the susceptibility to colitis in mice. However, the inflammasome sensor absent in melanoma 2 (AIM2) protects against colorectal cancer in an inflammasome-independent manner through DNA-dependent protein kinase and Akt pathways. Yet, the roles of the AIM2 inflammasome in IBD and the early phases of colorectal cancer remain ill-defined. Here we show that the AIM2 inflammasome has a protective role in the intestine. During steady state, Aim2 deletion results in the loss of IL-18 secretion, suppression of the IL-22 binding protein (IL-22BP) in intestinal epithelial cells and consequent loss of the STAT3-dependent antimicrobial peptides (AMPs) Reg3β and Reg3γ, which promotes dysbiosis-linked colitis. During dextran sulfate sodium-induced colitis, a dysfunctional IL-18/IL-22BP pathway in Aim2

Indexed as

HomeostasisSignal TransductionAnimalsAntigens, NeoplasmBacteriaBiomarkers, TumorColitisDextran SulfateDNA-Binding ProteinsDysbiosisEnterocytesInflammasomesInterleukin-18Interleukin-22InterleukinsIntestinal MucosaAim2 protein, mouseAntigens, NeoplasmBiomarkers, TumorDextran SulfateDNA-Binding ProteinsInflammasomesInterleukin-18Interleukin-22InterleukinsLectins, C-TypePancreatitis-Associated ProteinsPeptidesProteinsReg3b protein, mouseSTAT3 Transcription Factor

Identifiers

PMID27524110
PMCPMC5214942
OpenAlexW2507937615

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.