Evidence map›Paper›PMID 27693356›Full record

ArticleCell2016

IRGB10 Liberates Bacterial Ligands for Sensing by the AIM2 and Caspase-11-NLRP3 Inflammasomes.

Si Ming Man, Rajendra Karki, Miwa Sasai, David E Place, Sannula Kesavardhana, Jamshid Temirov, Sharon Frase, Qifan Zhu, R K Subbarao Malireddi, Teneema Kuriakose and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 207 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
207citing papers in PubMed, 1 pooled it
18.5field-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

207 citing papers in PubMed, 1 synthesis or guideline pooled it, 303 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
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  5. Article
  6. Article
  7. Review
  8. How to recognize if a cell dies from pyroptosis?Molecular biology reports · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Review
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  15. Article
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  18. Article
  19. Regulation of inflammatory processes by caspases.Nature reviews. Molecular cell biology · 2025
    Review
  20. Review

147 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 4 institutions in 2 countries.

Si Ming ManDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Rajendra KarkiDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Miwa SasaiDepartment of Immunoparasitology, Research Institute for Microbial Diseases, Laboratory of Immunoparasitology, World Premier International Immunology Frontier Research Center, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan.
David E PlaceDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Sannula KesavardhanaDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Jamshid TemirovDepartment of Cellular Imaging Shared Resource, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Sharon FraseCell and Tissue Imaging Center, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Qifan ZhuDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA; Integrated Biomedical Sciences Program, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
R K Subbarao MalireddiDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Teneema KuriakoseDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Jennifer L PetersDepartment of Cellular Imaging Shared Resource, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Geoffrey NealeHartwell Center for Bioinformatics & Biotechnology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Scott A BrownDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Masahiro YamamotoDepartment of Immunoparasitology, Research Institute for Microbial Diseases, Laboratory of Immunoparasitology, World Premier International Immunology Frontier Research Center, Osaka University, 3-1 Yamadaoka, Suita, Osaka 565-0871, Japan.
Thirumala-Devi KannegantiDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA. Electronic address: thirumala-devi.kanneganti@stjude.org.
St. Jude Children's Research Hospital · USImaging Center · USOsaka International University · JPOsaka University · JP

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
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 P30 CA021765NCI 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

The inflammasome is an intracellular signaling complex, which on recognition of pathogens and physiological aberration, drives activation of caspase-1, pyroptosis, and the release of the pro-inflammatory cytokines IL-1β and IL-18. Bacterial ligands must secure entry into the cytoplasm to activate inflammasomes; however, the mechanisms by which concealed ligands are liberated in the cytoplasm have remained unclear. Here, we showed that the interferon-inducible protein IRGB10 is essential for activation of the DNA-sensing AIM2 inflammasome by Francisella novicida and contributed to the activation of the LPS-sensing caspase-11 and NLRP3 inflammasome by Gram-negative bacteria. IRGB10 directly targeted cytoplasmic bacteria through a mechanism requiring guanylate-binding proteins. Localization of IRGB10 to the bacterial cell membrane compromised bacterial structural integrity and mediated cytosolic release of ligands for recognition by inflammasome sensors. Overall, our results reveal IRGB10 as part of a conserved signaling hub at the interface between cell-autonomous immunity and innate immune sensing pathways.

Indexed as

AnimalsB-LymphocytesCaspasesCaspases, InitiatorCytosolDNA-Binding ProteinsFrancisellaGram-Negative Bacterial InfectionsGTP PhosphohydrolasesHost-Pathogen InteractionsImmunity, CellularImmunity, InnateInflammasomesLigandsMiceMice, Mutant StrainsAim2 protein, mouseCasp4 protein, mouseCaspasesCaspases, InitiatorDNA-Binding ProteinsGTP PhosphohydrolasesInflammasomesIrgb10 protein, mouseLigandsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousecaspase-1cell-autonomous immunityGBP2GBP5GBPsimmunity-related GTPasesinnate immunityinterferonsLPSnon-canonical inflammasome

Identifiers

PMID27693356
PMCPMC5074697
OpenAlexW2524431814

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.