Evidence map›Paper›PMID 28191008›Full record

ReviewFrontiers in immunology2017

The NLRP3 and Pyrin Inflammasomes: Implications in the Pathophysiology of Autoinflammatory Diseases.

Carlos de Torre-Minguela, Pablo Mesa Del Castillo, Pablo Pelegrín

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed, 3 pooled it
12.3field-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

144 citing papers in PubMed, 3 syntheses or guidelines pooled it, 237 citations in OpenAlex.

  1. Pooled it
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  9. Frontiers in immunology · 2026
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  18. Functional interplay between non-canonical inflammasomes and autophagy in inflammatory responses and diseases.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
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  20. Review

84 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

3 authors at 2 institutions in 1 country.

Carlos de Torre-MinguelaUnidad de Inflamación Molecular, Instituto Murciano de Investigación Biosanitaria-Virgen de la Arrixaca (IMIB-Arrixaca), CIBERehd, Hospital Clínico Universitario Virgen de la Arrixaca , Murcia , Spain.
Pablo Mesa Del CastilloUnidad de Inflamación Molecular, Instituto Murciano de Investigación Biosanitaria-Virgen de la Arrixaca (IMIB-Arrixaca), CIBERehd, Hospital Clínico Universitario Virgen de la Arrixaca, Murcia, Spain; Unidad de Reumatología Pediátrica, Hospital Clínico Universitario Virgen de la Arrixaca, Murcia, Spain.
Pablo PelegrínUnidad de Inflamación Molecular, Instituto Murciano de Investigación Biosanitaria-Virgen de la Arrixaca (IMIB-Arrixaca), CIBERehd, Hospital Clínico Universitario Virgen de la Arrixaca , Murcia , Spain.
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ESHospital Universitario Virgen de la Arrixaca · ES

Funding

European Research Council 614578
6 · The paper itself

Abstract

Inflammasomes are multiprotein complexes that critically control different aspects of innate and adaptive immunity. Among them we could highlight the release of pro-inflammatory cytokines that induce and maintain the inflammatory response. Usually, inflammasomes result from oligomerization of a nucleotide-binding domain-like receptor (NLR) after sensing different pathogenic or endogenous sterile dangerous signals; however, other proteins such as absent in melanoma 2, retinoic acid-inducible gene I, or pyrin could also form inflammasome platforms. Inflammasome oligomerization leads to caspase-1 activation and the processing and release of the pro-inflammatory cytokines, such as interleukin (IL)-1β and IL-18. Mutations in different inflammasomes are causative for multiple periodic hereditary syndromes or autoinflammatory diseases, characterized by acute systemic inflammatory flares not associated with infections, tumors, or autoimmunity. This review focuses on germline mutations that have been described in cryopyrin-associated periodic syndrome (CAPS) for

Indexed as

cryopyrin-associated periodic syndromeextracellular ATPfamilial Mediterranean feverinflammationNLRP3P2X7 receptorpyrin

Identifiers

PMID28191008
PMCPMC5271383
OpenAlexW2581533407

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.