Evidence map›Paper›PMID 27997058›Full record

ReviewBrain pathology (Zurich, Switzerland)2017

Inflammasome activation in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE).

William Barclay, Mari L Shinohara

Open access · greenAbstract readReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

81 citing papers in PubMed, 154 citations in OpenAlex.

  1. The Roles of Interleukin-18 in Inflammation and Autoimmune Disease.Clinical reviews in allergy & immunology · 2026
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  17. Role of NLRP3 Inflammasomes in Neurodegenerative Diseases.The Eurasian journal of medicine · 2023
    Article
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  19. mScience China. Life sciences · 2023
    Article
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21 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 1 institution in 1 country.

William BarclayDepartment of Immunology, Duke University Medical School, Durham, NC.
Mari L ShinoharaDepartment of Immunology, Duke University Medical School, Durham, NC.ORCID 0000-0002-6808-9844
Duke University · US

Funding

Basic Immunology Training ProgramT32AI052077 · NIAID · DUKE UNIVERSITY · PI KRANGEL, MICHAEL S · 2002 to 2024
$4.2M
NIAID NIH HHS T32 AI052077
6 · The paper itself

Abstract

The aptly named inflammasomes are powerful signaling complexes that sense inflammatory signals under a myriad of conditions, including those from infections and endogenous sources. The inflammasomes promote inflammation by maturation and release of the pro-inflammatory cytokines, IL-1β and IL-18. Several inflammasomes have been identified so far, but this review focuses mainly on the NLRP3 inflammasome. By still ill-defined activation mechanisms, a sensor molecule, NLRP3 (NACHT, LRR and PYD domains-containing protein 3), responds to danger signals and rapidly recruits ASC (apoptosis-associated speck-like protein containing a CARD) and pro-caspase-1 to form a large oligomeric signaling platform-the inflammasome. Involvement of the NLRP3 inflammasome in infections, metabolic disorders, autoinflammation, and autoimmunity, underscores its position as a central player in sensing microbial and damage signals and coordinating pro-inflammatory immune responses. Indeed, evidence in patients with multiple sclerosis (MS) suggests inflammasome activation occurs during disease. Experiments with the mouse model of MS, experimental autoimmune encephalomyelitis (EAE), specifically describe the NLRP3 inflammasome as critical and necessary to disease development. This review discusses recent studies in EAE and MS which describe associations of inflammasome activation with promotion of T cell pathogenicity, infiltration of cells into the central nervous system (CNS) and direct neurodegeneration during EAE and MS.

Indexed as

AnimalsCarrier ProteinsCaspase 1Central Nervous SystemDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalHumansInflammasomesInflammationInterleukin-18Interleukin-1betaMiceMultiple SclerosisNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionCarrier ProteinsCaspase 1IL18 protein, humanInflammasomesInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 Proteinexperimental autoimmune encephalomyelitis (EAE)IFNβIL-1βinflammasomesmultiple sclerosis (MS)NLRP3

Identifiers

PMID27997058
PMCPMC8029098
OpenAlexW2562773331

What OpenQuestion holds

Textmetadata
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.