Evidence map›Paper›PMID 24165565›Full record

ReviewHuman vaccines & immunotherapeutics2014

Non-antigenic and antigenic interventions in type 1 diabetes.

Anna K E Rydén, Johnna D Wesley, Ken T Coppieters, Matthias G Von Herrath

Open access · hybridAbstract readReview
In one paragraph

Review in Human vaccines & immunotherapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

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  13. GABAergic system in the endocrine pancreas: a new target for diabetes treatment.Diabetes, metabolic syndrome and obesity : targets and therapy · 2015
    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 at 3 institutions in 2 countries.

Anna K E RydénType 1 Diabetes R&D Center; Novo Nordisk Inc.; Seattle, WA USA; Pacific Northwest Diabetes Research Institute; Seattle, WA USA.
Johnna D Wesley
Ken T Coppieters
Matthias G Von Herrath
Novo Nordisk (United States) · USNovo Nordisk (United Kingdom) · GBSeattle University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1D) results from autoimmune destruction of the pancreatic β-cells. Current T1D therapies are exclusively focused on regulating glycemia rather than the underlying immune response. A handful of trials have sought to alter the clinical course of T1D using various broad immune-suppressors, e.g., cyclosporine A and azathioprine.(1-3) The effect on β-cell preservation was significant, however, these therapies were associated with unacceptable side-effects. In contrast, more recent immunomodulators, such as anti-CD3 and antigenic therapies such as DiaPep277, provide a more targeted immunomodulation and have been generally well-tolerated and safe; however, as a monotherapy there appear to be limitations in terms of therapeutic benefit. Therefore, we argue that this new generation of immune-modifying agents will likely work best as part of a combination therapy. This review will summarize current immune-modulating therapies under investigation and discuss how to move the field of immunotherapy in T1D forward.

Indexed as

CD3 ComplexChaperonin 60Diabetes Mellitus, Type 1Drug Therapy, CombinationHumansImmunologic FactorsInsulinPeptide FragmentsTreatment OutcomeCD3 ComplexChaperonin 60DiaPep 277Immunologic FactorsInsulinPeptide FragmentsAnti-CD3Antigenic immune-modulationDiaPep277GAD65ImmunomodulationInsulinType 1 Diabetes

Identifiers

PMID24165565
PMCPMC4896560
OpenAlexW2017969352

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.