Evidence map›Paper›PMID 30185613›Full record

ReviewClinical science (London, England : 1979)2018

The classification, genetic diagnosis and modelling of monogenic autoinflammatory disorders.

Fiona Moghaddas, Seth L Masters

Open access · greenAbstract readReview
In one paragraph

Review in Clinical science (London, England : 1979), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

9 citing papers in PubMed, 31 citations in OpenAlex.

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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.

Fiona MoghaddasInflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia moghaddas.f@wehi.edu.au.
Seth L MastersInflammation Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, Australia.
University of Melbourne · AUWalter and Eliza Hall Institute of Medical Research · AU

Funding

Howard Hughes Medical InstituteWellcome Trust 208694/Z/17/Z
6 · The paper itself

Abstract

Monogenic autoinflammatory disorders are an increasingly heterogeneous group of conditions characterised by innate immune dysregulation. Improved genetic sequencing in recent years has led not only to the discovery of a plethora of conditions considered to be 'autoinflammatory', but also the broadening of the clinical and immunological phenotypic spectra seen in these disorders. This review outlines the classification strategies that have been employed for monogenic autoinflammatory disorders to date, including the primary innate immune pathway or the dominant cytokine implicated in disease pathogenesis, and highlights some of the advantages of these models. Furthermore, the use of the term 'autoinflammatory' is discussed in relation to disorders that cross the innate and adaptive immune divide. The utilisation of next-generation sequencing (NGS) in this population is examined, as are potential

Indexed as

CytokinesGenetic Association StudiesGenetic Predisposition to DiseaseHereditary Autoinflammatory DiseasesHumansImmunity, InnateInflammasomesInflammationMutationCytokinesInflammasomesAutoinflammatoryinflammasomeinterferonInterferonopathyPeriodic Fever Syndrome

Identifiers

PMID30185613
PMCPMC6123071
OpenAlexW2890670639

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.