Evidence map›Paper›PMID 27821552›Full record

ReviewThe Journal of experimental medicine2016

Type I interferon-mediated monogenic autoinflammation: The type I interferonopathies, a conceptual overview.

Mathieu P Rodero, Yanick J Crow

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 249 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
249citing papers in PubMed, 2 pooled it
19.1field-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

249 citing papers in PubMed, 2 syntheses or guidelines pooled it, 414 citations in OpenAlex.

  1. Pooled it
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  6. Therapeutic targeting of the cGAS-STING pathway in human disease.The Journal of clinical investigation · 2026
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189 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 2 countries.

Mathieu P RoderoINSERM UMR 1163, Laboratory of Neurogenetics and Neuroinflammation, 75015 Paris, France.ORCID 0000-0002-1300-0187
Yanick J CrowINSERM UMR 1163, Laboratory of Neurogenetics and Neuroinflammation, 75015 Paris, France yanickcrow@mac.com.ORCID 0000-0001-7211-7564
Délégation Paris 5 · FRInserm · FR

Funding

European Research Council 309449Medical Research Council MR/M501803/1
6 · The paper itself

Abstract

Type I interferon is a potent substance. As such, the induction, transmission, and resolution of the type I interferon-mediated immune response are tightly regulated. As defined, the type I interferonopathies represent discrete examples of a disturbance of the homeostatic control of this system caused by Mendelian mutations. Considering the complexity of the interferon response, the identification of further monogenic diseases belonging to this disease grouping seems likely, with the recognition of type I interferonopathies becoming of increasing clinical importance as treatment options are developed based on an understanding of disease pathology and innate immune signaling. Definition of the type I interferonopathies indicates that autoinflammation can be both interferon and noninterferon related, and that a primary disturbance of the innate immune system can "spill over" into autoimmunity in some cases. Indeed, that several non-Mendelian disorders, most particularly systemic lupus erythematosus and dermatomyositis, are also characterized by an up-regulation of type I interferon signaling suggests the possibility that insights derived from this work will have relevance to a broader field of clinical medicine.

Indexed as

AnimalsAutoimmunityHumansInflammationInterferon Type IModels, BiologicalPenetrancePhenotypeInterferon Type I

Identifiers

PMID27821552
PMCPMC5110029
OpenAlexW2556737993

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.