Evidence map›Paper›PMID 35451371›Full record

ArticleJCI insight2022

The AIM2 inflammasome is activated in astrocytes during the late phase of EAE.

William E Barclay, Nupur Aggarwal, M Elizabeth Deerhake, Makoto Inoue, Toshiaki Nonaka, Kengo Nozaki, Nathan A Luzum, Edward A Miao, Mari L Shinohara

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Inflammasomes in neurodegenerative diseases.Translational neurodegeneration · 2024
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. P2XBrain, behavior, and immunity · 2023
    Article
  20. Review
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

9 authors at 2 institutions in 1 country.

William E BarclayDepartment of Immunology, Duke University School of Medicine, Durham, North Carolina, USA.
Nupur AggarwalDepartment of Immunology, Duke University School of Medicine, Durham, North Carolina, USA.
M Elizabeth DeerhakeDepartment of Immunology, Duke University School of Medicine, Durham, North Carolina, USA.
Makoto InoueDepartment of Immunology, Duke University School of Medicine, Durham, North Carolina, USA.
Toshiaki NonakaDepartment of Immunology, Duke University School of Medicine, Durham, North Carolina, USA.
Kengo NozakiDepartment of Immunology, Duke University School of Medicine, Durham, North Carolina, USA.
Nathan A LuzumDepartment of Immunology, Duke University School of Medicine, Durham, North Carolina, USA.
Edward A MiaoDepartment of Immunology, Duke University School of Medicine, Durham, North Carolina, USA.
Mari L ShinoharaDepartment of Immunology, Duke University School of Medicine, Durham, North Carolina, USA.
Duke University · USUniversity of Illinois Urbana-Champaign · US

Funding

Role of osteopontin in innate immunity during infections and inflammationR01AI088100 · NIAID · DUKE UNIVERSITY · PI SHINOHARA, MARI L. · 2011 to 2021
$4.3M
Basic Immunology Training ProgramT32AI052077 · NIAID · DUKE UNIVERSITY · PI KRANGEL, MICHAEL S · 2002 to 2024
$4.2M
Protective role of Clec7a/dectin-1 in CNS autoimmunityR01NS120417 · NINDS · DUKE UNIVERSITY · PI SHINOHARA, MARI L. · 2021 to 2025
$2.0M
NIAID NIH HHS R01 AI088100NIAID NIH HHS T32 AI052077NINDS NIH HHS R01 NS120417
6 · The paper itself

Abstract

Inflammasomes are a class of innate immune signaling platforms that activate in response to an array of cellular damage and pathogens. Inflammasomes promote inflammation under many circumstances to enhance immunity against pathogens and inflammatory responses through their effector cytokines, IL-1β and IL-18. Multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), are autoimmune conditions influenced by inflammasomes. Despite work investigating inflammasomes during EAE, little remains known concerning the role of inflammasomes in the central nervous system (CNS) during the disease. Here, we used multiple genetically modified mouse models to monitor activated inflammasomes in situ based on oligomerization of apoptosis-associated speck-like protein containing a CARD (ASC) in the spinal cord. Using inflammasome reporter mice, we found heightened inflammasome activation in astrocytes after the disease peak. In contrast, microglia and CNS-infiltrated myeloid cells had few activated inflammasomes in the CNS during EAE. Astrocyte inflammasome activation during EAE was dependent on absent in melanoma 2 (AIM2), but low IL-1β release and no significant signs of cell death were found. Thus, the AIM2 inflammasome activation in astrocytes may have a distinct role from traditional inflammasome-mediated inflammation.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMelanomaAnimalsAstrocytesDisease Models, AnimalDNA-Binding ProteinsInflammasomesInflammationMiceNLR Family, Pyrin Domain-Containing 3 ProteinAim2 protein, mouseDNA-Binding ProteinsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinAutoimmune diseasesAutoimmunityInnate immunityMultiple sclerosisNeuroscience

Identifiers

PMID35451371
PMCPMC9089781
OpenAlexW4224233385

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.