Evidence map›Paper›PMID 23209415›Full record

ArticlePLoS pathogens2012

Molecular anatomy and number of antigen specific CD8 T cells required to cause type 1 diabetes.

Michael B A Oldstone, Kurt H Edelmann, Dorian B McGavern, Justin T Cruite, Megan J Welch

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Gut-tropic α4β7Frontiers in immunology · 2025
    Article
  2. One in Ten CD8Diabetes · 2021
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Progression of type 1 diabetes from the prediabetic stage is controlled by interferon-α signaling.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. 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

5 authors at 1 institution in 1 country.

Michael B A OldstoneViral-Immunobiology Laboratory, Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California, United States of America. mbaobo@scripps.edu
Kurt H Edelmann
Dorian B McGavern
Justin T Cruite
Megan J Welch
Scripps Research Institute · US

Funding

Pathogenesis of viral meningitisZIANS003112 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI MCGAVERN, DORIAN · 2009 to 2025
$33.6M
PATHOGENESIS OF PERSISTENT VIRAL INFECTIONR01AI009484 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI OLDSTONE, MICHAEL B · 1985 to 2016
$7.2M
In Vivo Analysis of T lymphocytes in the Persistently Infected CNSR01AI070967 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI OLDSTONE, MICHAEL B · 2007 to 2011
$2.3M
PATHOGENESIS OF PERSISTENT VIRAL INFECTIONR37AI009484 · NIAID · SCRIPPS RESEARCH INSTITUTE · PI OLDSTONE, MICHAEL B · 1988 to 1997
–
NIAID NIH HHS AI009484NIAID NIH HHS AI070967NIAID NIH HHS R01 AI009484NIAID NIH HHS R01 AI070967
6 · The paper itself

Abstract

We quantified CD8 T cells needed to cause type 1 diabetes and studied the anatomy of the CD8 T cell/beta (β) cell interaction at the immunologic synapse. We used a transgenic model, in situ tetramer staining to distinguish antigen specific CD8 T cells from total T cells infiltrating islets and a variety of viral mutants selected for functional deletion(s) of various CD8 T cell epitopes. Twenty percent of CD8 T cells in the spleen were specific for all immunodominant and subdominant viral glycoprotein (GP) epitopes. CTLs to the immunodominant LCMV GP33-41 epitope accounted for 63% of the total (12.5% of tetramers). In situ hybridization analysis demonstrated only 1 to 2% of total infiltrating CD8 T cells were specific for GP33 CD8 T cell epitope, yet diabetes occurred in 94% of mice. The immunologic synapse between GP33 CD8 CTL and β cell contained LFA-1 and perforin. Silencing both immunodominant epitopes (GP33, GP276-286) in the infecting virus led to a four-fold reduction in viral specific CD8 CTL responses, negligible lymphocyte infiltration into islets and absence of diabetes.

Indexed as

AnimalsCD8-Positive T-LymphocytesDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Immunodominant EpitopesImmunological SynapsesInsulin-Secreting CellsMiceMice, TransgenicReceptors, Antigen, T-Cell, alpha-betaImmunodominant EpitopesReceptors, Antigen, T-Cell, alpha-beta

Identifiers

PMID23209415
PMCPMC3510245
OpenAlexW2063480188

What OpenQuestion holds

Textmetadata
LicenceCC0
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.