Evidence map›Paper›PMID 22956469›Full record

ReviewImmunologic research2013

Type 1 diabetes: primary antigen/peptide/register/trimolecular complex.

Tomasz Sosinowski, George S Eisenbarth

Open access · greenAbstract readReview
In one paragraph

Review in Immunologic research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. The yin/yang balance of the MHC-selfFrontiers in immunology · 2022
    Review
  2. Article
  3. Article
  4. Article
  5. T Cell Receptor Profiling in Type 1 Diabetes.Current diabetes reports · 2017
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Chemical methods for peptide and protein production.Molecules (Basel, Switzerland) · 2013
    Review
  14. 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

2 authors at 1 institution in 1 country.

Tomasz SosinowskiBarbara Davis Center for Childhood Diabetes, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA. Tomasz.sosinowski@ucdenver.edu
George S Eisenbarth
University of Colorado Anschutz Medical Campus · US

Funding

Immune Tolerance Network: Type 1 diabetesN01AI15416 · NIAID · UNIVERSITY OF SAN FRANCISCO · PI BLUESTONE, JEFFREY · 2007 to 2013
$276.6M
Virginia Mason/UCHSC Autoimmune Prevention CenterU19AI050864 · NIAID · UNIVERSITY OF COLORADO DENVER · PI HOLERS, VERNON MICHAEL · 2001 to 2011
$29.2M
UCHSC DIABETES ENDOCRINOLOGY RESEARCH CENTERP30DK057516 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI HUTTON, JOHN C · 2000 to 2010
$14.0M
Multiple Autoantigens/Multiple Epitopes of Type 1DMR01DK032083 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI MICHELS, AARON W · 1986 to 2025
$6.9M
IMMUNE TOLERANCE NETWORK-266015416-266015416N01AI015416 · NIAID · REGENTS OF THE UNIVERSITY OF C · PI BLUESTONE, JEFFREY A · 2002 to 2006
–
NIAID NIH HHS N01 AI015416NIAID NIH HHS N01 AI 15416NIAID NIH HHS U19 AI050864NIAID NIH HHS U19AI050864NIDDK NIH HHS P30 DK057516NIDDK NIH HHS R01 DK 032083NIDDK NIH HHS R01 DK032083
6 · The paper itself

Abstract

Type 1A diabetes (autoimmune) is now immunologically predictable in man, but preventable only in animal models. What triggers the development of autoimmunity in genetically susceptible individuals remains unknown. Studies of non-obese diabetic (NOD) mice reveal that interactions between T-cell receptors of diabetogenic T cell and an MHC class II loaded with an autoantigen are key determinates of the disease. With insulin as the primary target in the NOD mouse, likely man, and possibly the RT1-U rat models, therapeutic targeting of the components of these anti-insulin trimolecular complexes we believe provide a fulcrum for development of preventive therapy. In particular for the NOD mouse model, there is extensive evidence that the dominant insulin peptide driving disease initiation is insulin B chain amino acids 9-23 (SHLVEALYLVCGERG) recognized predominantly by germ-line sequences of a specific T-cell receptor Valpha (TRAV5D-4), and small molecules or monoclonal antibodies directed at this recognition complex can prevent diabetes.

Indexed as

AnimalsAutoantigensDiabetes Mellitus, Type 1Genes, MHC Class IIHumansPeptidesReceptors, Antigen, T-CellAutoantigensPeptidesReceptors, Antigen, T-Cell

Identifiers

PMID22956469
PMCPMC3936464
OpenAlexW2143031309

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.