Evidence map›Paper›PMID 16306940›Full record

ArticleNature2005

Immunology: Insulin auto-antigenicity in type 1 diabetes.

Darcy B Wilson

Open access · bronzeAbstract readComment
PubMed Publisher
In one paragraph

Article in Nature, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. A Single L/D-Substitution at Q4 of the mInsAFrontiers in immunology · 2021
    Article
  3. Article
  4. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Darcy B WilsonTorrey Pines Institute for Molecular Studies, San Diego, California 92121-1122, USA. dbwilson@tpims.org
Torrey Pines Institute For Molecular Studies · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spontaneous type 1 diabetes occurs when the autoimmune destruction of pancreatic beta-islet cells prevents production of the hormone insulin. This causes an inability to regulate glucose metabolism, which results in dangerously raised blood glucose concentrations. It is generally accepted that thymus-derived lymphocytes (T cells) are critically involved in the onset and progression of type 1 diabetes, but the antigens that initiate and drive this destructive process remain poorly characterized--although several candidates have been considered. Nakayama et al. and Kent et al. claim that insulin itself is the primary autoantigen that initiates spontaneous type 1 diabetes in mice and humans, respectively, a result that could have implications for more effective prevention and therapy. However, I believe that this proposed immunological role of insulin may be undermined by the atypical responses of T cells to the human insulin fragment that are described by Kent et al..

Indexed as

Models, ImmunologicalAnimalsAutoantigensAutoimmunityCross ReactionsDiabetes Mellitus, Type 1Disease Models, AnimalHumansInsulinInsulin SecretionIslets of LangerhansLymph NodesMicePeptide FragmentsReproducibility of ResultsT-LymphocytesAutoantigensInsulinPeptide Fragments

Identifiers

PMID16306940
OpenAlexW2090638161

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.