Evidence map›Paper›PMID 28835461›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2017

Ectopic Expression of Self-Antigen Drives Regulatory T Cell Development and Not Deletion of Autoimmune T Cells.

Thomas Lee, Maran L Sprouse, Pinaki Banerjee, Maria Bettini, Matthew L Bettini

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2017. 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
1.3field-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, 16 citations in OpenAlex.

  1. Increased Nur77 is disconnected from TCR affinity in insulin-specific Tregs.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Article
  2. Article
  3. Review
  4. De novo identification of CD4Nature methods · 2024
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Generation of T Cell Receptor Retrogenic Mice.Current protocols in immunology · 2019
    Article
  13. 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

5 authors at 1 institution in 1 country.

Thomas LeeSection of Diabetes and Endocrinology, Department of Pediatrics, Baylor College of Medicine, Texas Children's Hospital, Houston, TX 77030; and.
Maran L SprouseSection of Diabetes and Endocrinology, Department of Pediatrics, Baylor College of Medicine, Texas Children's Hospital, Houston, TX 77030; and.ORCID 0000-0002-4017-8466
Pinaki BanerjeeCenter for Human Immunobiology, Baylor College of Medicine, Texas Children's Hospital, Houston, TX 77030.
Maria BettiniSection of Diabetes and Endocrinology, Department of Pediatrics, Baylor College of Medicine, Texas Children's Hospital, Houston, TX 77030; and.ORCID 0000-0002-6415-7731
Matthew L BettiniSection of Diabetes and Endocrinology, Department of Pediatrics, Baylor College of Medicine, Texas Children's Hospital, Houston, TX 77030; and matthew.bettini@bcm.edu.ORCID 0000-0001-5596-186X
Baylor College of Medicine · US

Funding

TCR PARAMETERS OF TREG FUNCTION IN AUTOIMMUNITYR01AI125301 · NIAID · UNIVERSITY OF UTAH · PI BETTINI, MARIA · 2017 to 2021
$1.9M
Parameters T-Cell Receptor avidity during thymic selection in autoimmune diabetesK22AI104761 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI BETTINI, MATTHEW · 2014 to 2015
$269k
Self-Reactive T Cell Development in Type 1 DiabetesR56DK104903 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI BETTINI, MATTHEW · 2015 to 2015
$158k
NIAID NIH HHS K22 AI104761NIAID NIH HHS R01 AI125301NIDDK NIH HHS R56 DK104903
6 · The paper itself

Abstract

Type 1 diabetes is a T cell-mediated autoimmune disease that is characterized by Ag-specific targeting and destruction of insulin-producing β cells. Although multiple studies have characterized the pathogenic potential of β cell-specific T cells, we have limited mechanistic insight into self-reactive autoimmune T cell development and their escape from negative selection in the thymus. In this study, we demonstrate that ectopic expression of insulin epitope B:9-23 (InsB

Indexed as

AutoimmunityEctopic Gene ExpressionAnimalsAutoantigensAutoimmune DiseasesCD4-Positive T-LymphocytesCell DifferentiationDiabetes Mellitus, Type 1InsulinInsulin-Secreting CellsMicePeptide FragmentsThymocytesT-Lymphocytes, RegulatoryAutoantigensInsulininsulin B (9-23)Peptide Fragments

Identifiers

PMID28835461
PMCPMC5605461
OpenAlexW2745533849

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.