Evidence map›Paper›PMID 30115527›Full record

ReviewJournal of autoimmunity2018

Interferon alpha: The key trigger of type 1 diabetes.

Angela Lombardi, Effie Tsomos, Sara S Hammerstad, Yaron Tomer

Open access · greenAbstract readReview
In one paragraph

Review in Journal of autoimmunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
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  19. The immunology of type 1 diabetes.Nature reviews. Immunology · 2024
    Review
  20. Article
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 2 institutions in 2 countries.

Angela LombardiDepartment of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA. Electronic address: angela.lombardi@einstein.yu.edu.
Effie TsomosDepartment of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA.
Sara S HammerstadDepartment of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Aker, Oslo, Norway; Department of Pediatrics, Oslo University Hospital, Ulleval, Oslo, Norway.
Yaron TomerDepartment of Medicine, Albert Einstein College of Medicine, Bronx, NY, USA. Electronic address: ytomer@montefiore.org.
Albert Einstein College of Medicine · USOslo University Hospital · NO

Funding

Mapping Autoimmune Diabetes and Thyroiditis GenesR01DK067555 · NIDDK · UNIVERSITY OF CINCINNATI · PI MIHAELA STEFAN LIFSHITZ, YARON TOMER · 2005 to 2026
$5.8M
NIDDK NIH HHS R01 DK067555
6 · The paper itself

Abstract

IFNα is a cytokine essential to a vast array of immunologic processes. Its induction early in the innate immune response provides a priming mechanism that orchestrates numerous subsequent pathways in innate and adaptive immunity. Despite its beneficial effects in viral infections IFNα has been reported to be associated with several autoimmune diseases including autoimmune thyroid disease, systemic lupus erythematosus, rheumatoid arthritis, primary biliary cholangitis, and recently emerged as a major cytokine that triggers Type 1 Diabetes. In this review, we dissect the role of IFNα in T1D, focusing on the potential pathophysiological mechanisms involved. Evidence from human and mouse studies indicates that IFNα plays a key role in enhancing islet expression of HLA-I in patients with T1D, thereby increasing autoantigen presentation and beta cell activation of autoreactive cytotoxic CD8 T-lymphocytes. The binding of IFNα to its receptor induces the secretion of chemokines, attracting monocytes, T lymphocytes, and NK cells to the infected tissue triggering autoimmunity in susceptible individuals. Furthermore, IFNα impairs insulin production through the induction of endoplasmic reticulum stress as well as by impairing mitochondrial function. Due to its central role in the early phases of beta cell death, targeting IFNα and its pathways in genetically predisposed individuals may represent a potential novel therapeutic strategy in the very early stages of T1D.

Indexed as

AnimalsAntibodies, NeutralizingAutoantigensAutoimmunityChemokinesDiabetes Mellitus, Type 1Endoplasmic Reticulum StressGene Expression RegulationHumansInsulinInsulin-Secreting CellsInterferon-alphaKiller Cells, NaturalMiceMitochondriaMolecular Targeted TherapyAntibodies, NeutralizingAutoantigensChemokinesInsulinInterferon-alphaReceptor, Interferon alpha-betaInterferon alphaType 1 diabetes

Identifiers

PMID30115527
PMCPMC6235162
OpenAlexW2885090944

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.