Evidence map›Paper›PMID 30030289›Full record

ReviewDiabetes2018

Altered Function of Antigen-Presenting Cells in Type 1 Diabetes: A Challenge for Antigen-Specific Immunotherapy?

Rémi J Creusot, Jorge Postigo-Fernandez, Nato Teteloshvili

Open access · bronzeAbstract readReview
In one paragraph

Review in Diabetes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

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  11. Frontiers in endocrinology · 2022
    Review
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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 1 institution in 1 country.

Rémi J CreusotColumbia Center for Translational Immunology, Naomi Berrie Diabetes Center and Department of Medicine, Columbia University Medical Center, New York, NY rjc2150@columbia.edu.ORCID 0000-0002-8328-8155
Jorge Postigo-FernandezColumbia Center for Translational Immunology, Naomi Berrie Diabetes Center and Department of Medicine, Columbia University Medical Center, New York, NY.
Nato TeteloshviliColumbia Center for Translational Immunology, Naomi Berrie Diabetes Center and Department of Medicine, Columbia University Medical Center, New York, NY.
Columbia University Irving Medical Center · US

Funding

Engineering and targeting novel antigen-specific tolerogenic interfacesR21AI110812 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI CREUSOT, REMI J · 2015 to 2016
$440k
NIAID NIH HHS R21 AI110812
6 · The paper itself

Abstract

Type 1 diabetes (T1D) arises from a failure to maintain tolerance to specific β-cell antigens. Antigen-specific immunotherapy (ASIT) aims to reestablish immune tolerance through the supply of pertinent antigens to specific cell types or environments that are suitable for eliciting tolerogenic responses. However, antigen-presenting cells (APCs) in T1D patients and in animal models of T1D are affected by a number of alterations, some due to genetic polymorphism. Combination of these alterations, impacting the number, phenotype, and function of APC subsets, may account for both the underlying tolerance deficiency and for the limited efficacy of ASITs so far. In this comprehensive review, we examine different aspects of APC function that are pertinent to tolerance induction and summarize how they are altered in the context of T1D. We attempt to reconcile 25 years of studies on this topic, highlighting genetic, phenotypic, and functional features that are common or distinct between humans and animal models. Finally, we discuss the implications of these defects and the challenges they might pose for the use of ASITs to treat T1D. Better understanding of these APC alterations will help us design more efficient ways to induce tolerance.

Indexed as

Models, ImmunologicalAnimalsAntigen PresentationAntigen-Presenting CellsAutoantibodiesAutoimmune DiseasesAutoimmunityChemotaxisDiabetes Mellitus, Type 1Genetic Predisposition to DiseaseHumansHypoglycemic AgentsImmunotherapyPhagocytosisPolymorphism, GeneticAutoantibodiesHypoglycemic Agents

Identifiers

PMID30030289
PMCPMC6054431
OpenAlexW2883151650

What Socratic 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 Socratic graph.