Evidence map›Paper›PMID 29247997›Full record

ReviewImmunological reviews2018

The NLRC4 Inflammasome.

Joseph A Duncan, Scott W Canna

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 198 papers.

0numbers the graph read from it
0cells of the map it votes in
198citing papers in PubMed
12.1field-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

198 citing papers in PubMed, 302 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Toward targeting of inflammasome signaling in venous thrombosis.Journal of thrombosis and haemostasis : JTH · 2025
    Review

138 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.

Joseph A DuncanDivision of Infectious Diseases, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Scott W CannaPediatric Rheumatology & RK Mellon Institute for Pediatric Research, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA, USA.ORCID 0000-0003-3837-5337
Children's Hospital of Pittsburgh · USUniversity of North Carolina at Chapel Hill · US

Funding

Regulation of the physiologic and pathologic activation of the NLRP3-inflammasomeR01AI088255 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DUNCAN, JOSEPH A · 2010 to 2020
$3.9M
Mechanisms of NLRC4 inflammasome-associated hyperinflammationK22AI123366 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CANNA, SCOTT WILLIAM · 2017 to 2018
$270k
NIAID NIH HHS K22 AI123366NIAID NIH HHS R01 AI088255
6 · The paper itself

Abstract

15 years ago, the fundamental biology of an inflammatory signaling complex eventually dubbed "the inflammasome" began to unravel in chronologic parallel with the discovery that many inflammatory diseases were associated with its hyperactivity. Though the genetic origins of Familial Mediterranean Fever (FMF, caused my mutations in MEFV) were discovered first, it would take nearly two decades before the mechanistic connections to a PYRIN inflammasome were made. In the interim, the intensive study of the NLRP3 inflammasome, and the diseases associated with its hyperactivation, have largely dictated the paradigm of inflammasome composition and function. Despite impressive gains, focusing on NLRP3 left gaps in our understanding of inflammasome biology. Foremost among these gaps were how inflammasomes become activated and the connections between inflammasome structure and function. Fortunately, work in another inflammasome inducer, NLRC4, grew to fill those gaps. The current understanding of the NLRC4 inflammasome is perhaps the most comprehensive illustration of the inflammasome paradigm: trigger (e.g. cytosolic flagellin), sensor (NAIP), nucleator (NLRC4), adaptor (ASC), and effector (CASP1). Detailed work has also identified observations that challenge this paradigm. Simultaneously, the features unique to each inflammasome offer a lesson in contrast, providing perspectives on inflammasome activation, regulation, and function. In this review, we endeavor to highlight recent breakthroughs related to NLRC4 inflammasome structure and activation, important in vivo work in infection and systemic inflammation, and the characterization of a spectrum of human NLRC4-associated autoinflammatory diseases.

Indexed as

AnimalsAutoimmune DiseasesCalcium-Binding ProteinsCARD Signaling Adaptor ProteinsFamilial Mediterranean FeverHumansInfectionsInflammasomesInflammationPyrinSignal TransductionCalcium-Binding ProteinsCARD Signaling Adaptor ProteinsInflammasomesNLRC4 protein, humanPyrinAutoinflammationInflammasomeInflammationinterleukin-18

Identifiers

PMID29247997
PMCPMC5897049
OpenAlexW2778837083

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.