Evidence map›Paper›PMID 22393537›Full record

ReviewCold Spring Harbor perspectives in medicine2012

Breakdown in peripheral tolerance in type 1 diabetes in mice and humans.

Lukas T Jeker, Hélène Bour-Jordan, Jeffrey A Bluestone

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing 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

53 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. Altered B cell metabolic pathways characterize type 1 diabetes progression.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Article
  3. Extracellular vesicles fromFrontiers in immunology · 2026
    Article
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  9. Aire mediates tolerance to insulin through thymic trimming of high-affinity T cell clones.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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.

Lukas T JekerUCSF Diabetes Center, University of California at San Francisco, San Francisco, California 94143, USA.
Hélène Bour-Jordan
Jeffrey A Bluestone
University of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 Diabetes (T1D), also called juvenile diabetes because of its classically early onset, is considered an autoimmune disease targeting the insulin-producing β cells in the pancreatic islets of Langerhans. T1D reflects a loss of tolerance to tissue self-antigens caused by defects in both central tolerance, which aims at eliminating potentially autoreactive lymphocytes developing in the thymus, and peripheral tolerance, which normally controls autoreactive T cells that escaped the thymus. Like in other autoimmune diseases, the mechanisms leading to T1D are multifactorial and depend on a complex combination of genetic, epigenetic, molecular, and cellular elements that result in the breakdown of peripheral tolerance. In this article, we discuss the contribution of these factors in the development of the autoimmune response targeting pancreatic islets in T1D and the therapeutic strategies currently being explored to correct these defects.

Indexed as

AnimalsAutoantigensAutoimmunityCTLA-4 AntigenDiabetes Mellitus, Type 1Disease ProgressionGenome-Wide Association StudyHumansInterleukin-2Islets of LangerhansMiceMice, Inbred NODPeripheral ToleranceT-Lymphocytes, RegulatoryAutoantigensCTLA-4 AntigenInterleukin-2

Identifiers

PMID22393537
PMCPMC3282496
OpenAlexW2102542457

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.