Evidence map›Paper›PMID 22504578›Full record

ReviewCurrent opinion in rheumatology2012

Infection as a cause of type 1 diabetes?

Urs Christen, Christine Bender, Matthias G von Herrath

Abstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 53 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

3 authors at 2 institutions in 2 countries.

Urs ChristenPharmazentrum Frankfurt / ZAFES, Goethe University Hospital, Frankfurt am Main, Germany. christen@med.uni-frankfurt.de
Christine Bender
Matthias G von Herrath
Goethe University Frankfurt · DELa Jolla Institute for Immunology · US

Funding

Treg stability in viral infection and autoimmunityP01AI089624 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI PETERS, BJOERN · 2010 to 2014
$10.1M
NIAID NIH HHS P01 AI089624
6 · The paper itself

Abstract

purpose of reviewIt is the current opinion that pathogens, such as viruses, are contributing to the development of type 1 diabetes (T1D) in susceptible individuals. This opinion is based on epidemiological associations, direct isolation of pathogens from the islets of Langerhans, as well as a large amount of data from various experimental animal models. Human enteroviruses have dominated the literature associated with the etiology of T1D. However, virus infections have also been reported to protect from autoimmune disorders. RECENT

findingsHere we review the evidence for virus infections to be involved in the pathogenesis of T1D and discuss potential mechanisms of how such infections could accelerate the destruction of insulin-producing β-cells. In addition, we will review evidence from epidemiologic and experimental animal studies showing that virus infections could also have protective properties. SUMMARY: Virus infections play an important role in the pathogenesis of T1D by inducing or accelerating the autodestructive process, but also by protecting from autoimmunity. Thus, multiple sequential infections might shape the autoreactive immune repertoire and the pathogenesis of T1D in a complex fashion.

Indexed as

AnimalsDiabetes Mellitus, Type 1Disease Models, AnimalEnterovirus InfectionsEvidence-Based MedicineHumansIslets of LangerhansMolecular MimicryVirus Diseases

Identifiers

PMID22504578
PMCPMC4828240
OpenAlexW2080559919

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.