Evidence map›Paper›PMID 26744186›Full record

ReviewZeitschrift fur Rheumatologie2016

[Type I interferonopathies. Systemic inflammatory diseases triggered by type I interferons].

C Günther, F Schmidt, N König, M A Lee-Kirsch

Abstract readReview
PubMed Publisher
In one paragraph

Review in Zeitschrift fur Rheumatologie, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
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

4 authors.

C GüntherKlinik für Dermatologie, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Deutschland. claudia.guenther@uniklinikum-dresden.de.
F SchmidtKlinik für Dermatologie, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 74, 01307, Dresden, Deutschland.
N KönigKlinik für Kinder- und Jugendmedizin, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Dresden, Deutschland.
M A Lee-KirschKlinik für Kinder- und Jugendmedizin, Medizinische Fakultät Carl Gustav Carus, Technische Universität Dresden, Dresden, Deutschland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I interferons mediate immune defense against viral infections. The induction of type I interferons has stimulating and modulating effects on the innate and adaptive immune systems thereby reducing tolerance against self-antigens. Genetic defects that result in an inadequate activation of the type I interferon system can cause a group of inflammatory disorders, which are collectively referred to as type I interferonopathies. While the clinical spectrum of type I interferonopathies is broad and heterogeneous, neurological and cutaneous symptoms are the most frequent manifestations. Some clinical and genetic features of type I interferonopathies are shared by multifactorial diseases, such as systemic lupus erythematosus and systemic vasculitis. Advances in understanding the disease mechanisms underlying type I interferonopathies have pinpointed novel targets for therapeutic interventions.

Indexed as

Autoimmune DiseasesDisease SusceptibilityHereditary Autoinflammatory DiseasesHost-Pathogen InteractionsHumansInterferon Type IRare DiseasesInterferon Type IAutoimmunityAutoinflammationImmune systemMonogenic diseasesSystemic lupus erythematosus

Identifiers

PMID26744186

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.