Evidence map›Paper›PMID 22647732›Full record

ArticleJournal of autoimmunity2012

Pathogenesis of NOD diabetes is initiated by reactivity to the insulin B chain 9-23 epitope and involves functional epitope spreading.

Suchitra Prasad, Adam P Kohm, Jeffrey S McMahon, Xunrong Luo, Stephen D Miller

Abstract read
In one paragraph

Article in Journal of autoimmunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

71 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Antigen-specific immunotherapy with a CD4Nature communications · 2026
    Article
  5. Article
  6. De novo identification of CD4Nature methods · 2024
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Vaccines for immune tolerance against autoimmune disease.Advanced drug delivery reviews · 2023
    Review
  12. Review
  13. Review
  14. Advanced Delivery Strategies for Immunotherapy in Type I Diabetes Mellitus.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2023
    Review
  15. Review
  16. Review
  17. Article
  18. T cell help in the autoreactive germinal center.Scandinavian journal of immunology · 2022
    Review
  19. Article
  20. Article

11 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Suchitra PrasadDepartment of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Adam P Kohm
Jeffrey S McMahon
Xunrong Luo
Stephen D Miller
Northwestern University · US

Funding

Multidisciplinary Clinical and Translational Science (MCTS) Program (UL1)UL1TR000150 · NCATS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LLOYD-JONES, DONALD M · 2012 to 2013
$10.1M
IMMUNOREGULATION AND PATHOLOGY OF CHRONIC-RELAPSING EAER01NS026543 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 1988 to 2016
$5.0M
Mechanisms of CD4+CD25+ T Regulatory Cells in EAER01NS048411 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 2005 to 2008
$1.3M
NCATS NIH HHS UL1 TR000150NINDS NIH HHS R01 NS-026543NINDS NIH HHS R01 NS026543NINDS NIH HHS R01 NS048411
6 · The paper itself

Abstract

Type 1 diabetes (T1D) is mediated by destruction of pancreatic β-cells by CD4 and CD8 T cells specific for epitopes on numerous diabetogenic autoantigens resulting in loss of glucose homeostasis. Employing antigen-specific tolerance induced by i.v. administration of syngeneic splenocytes ECDI cross-linked to various diabetogenic antigens/epitopes (Ag-SP), we show that epitope spreading plays a functional role in the pathogenesis of T1D in NOD mice. Specifically, Ag-SP coupled with intact insulin, Ins B(9-23) or Ins B(15-23), but not GAD65(509-528), GAD65(524-543) or IGRP(206-214), protected 4-6 week old NOD mice from the eventual development of clinical disease; infiltration of immune cells to the pancreatic islets; and blocked the induction of DTH responses in a Treg-dependent, antigen-specific manner. However, tolerance induction in 19-21 week old NOD mice was effectively accomplished only by Ins-SP, suggesting Ins B(9-23) is a dominant initiating epitope, but autoimmune responses to insulin epitope(s) distinct from Ins B(9-23) emerge during disease progression.

Indexed as

AutoimmunityAnimalsAutoantigensCell MovementCross-Linking ReagentsDiabetes Mellitus, Type 1Disease ProgressionEpitopesFemaleGlucose-6-PhosphataseGlutamate DecarboxylaseImmune ToleranceInjections, IntravenousInsulinInsulin-Secreting CellsMiceAutoantigensCross-Linking ReagentsEpitopesG6pc2 protein, mouseGlucose-6-PhosphataseGlutamate DecarboxylaseInsulininsulin B (9-23)Peptide FragmentsProteins

Identifiers

PMID22647732
PMCPMC3434243
OpenAlexW1992802035

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.