Evidence map›Paper›PMID 31836691›Full record

ArticleDiabetes2020

A Critical Insulin TCR Contact Residue Selects High-Affinity and Pathogenic Insulin-Specific T Cells.

Maria Bettini, Marissa A Scavuzzo, Baoyu Liu, Elizabeth Kolawole, Lin Guo, Brian D Evavold, Malgorzata Borowiak, Matthew L Bettini

Open access · greenAbstract read
In one paragraph

Article in Diabetes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Increased Nur77 is disconnected from TCR affinity in insulin-specific Tregs.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Article
  2. Review
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  10. Relationship of 2D Affinity to T Cell Functional Outcomes.International journal of molecular sciences · 2020
    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

8 authors at 2 institutions in 1 country.

Maria BettiniDepartment of Pediatrics, Baylor College of Medicine, Houston, TX matt.bettini@path.utah.edu maria.bettini@path.utah.edu.ORCID 0000-0002-6415-7731
Marissa A ScavuzzoProgram in Developmental Biology, Baylor College of Medicine, Houston, TX.
Baoyu LiuDivision of Microbiology and Immunology, Department of Pathology, University of Utah, Salt Lake City, UT.
Elizabeth KolawoleDivision of Microbiology and Immunology, Department of Pathology, University of Utah, Salt Lake City, UT.
Lin GuoDepartment of Pediatrics, Baylor College of Medicine, Houston, TX.
Brian D EvavoldDivision of Microbiology and Immunology, Department of Pathology, University of Utah, Salt Lake City, UT.ORCID 0000-0002-3561-3494
Malgorzata BorowiakMcNair Medical Institute, Texas Children's Hospital, Baylor College of Medicine, Houston, TX.
Matthew L BettiniDepartment of Pediatrics, Baylor College of Medicine, Houston, TX matt.bettini@path.utah.edu maria.bettini@path.utah.edu.ORCID 0000-0001-5596-186X
Baylor College of Medicine · USUniversity of Utah · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI Michael M Ittmann · 2007 to 2026
$73.9M
Virology CoreP30AI036211 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI KLINE, MARK W. · 1994 to 2015
$21.7M
TCR PARAMETERS OF TREG FUNCTION IN AUTOIMMUNITYR01AI125301 · NIAID · UNIVERSITY OF UTAH · PI BETTINI, MARIA · 2017 to 2021
$1.9M
Self-Reactive T Cell Development in Type 1 DiabetesR01DK114456 · NIDDK · UNIVERSITY OF UTAH · PI BETTINI, MATTHEW · 2018 to 2022
$1.9M
BD Biosciences Special Order LSRIIS10RR024574 · NCRR · BAYLOR COLLEGE OF MEDICINE · PI LUMPKIN, ELLEN A · 2009 to 2009
$430k
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
NCI NIH HHS P30 CA125123NCRR NIH HHS S10 RR024574NIAID NIH HHS K22 AI104761NIAID NIH HHS P30 AI036211NIAID NIH HHS R01 AI125301NIDDK NIH HHS R01 DK114456NIDDK NIH HHS R56 DK104903
6 · The paper itself

Abstract

Type 1 diabetes is an autoimmune-mediated disease that culminates in the targeted destruction of insulin-producing β-cells. CD4 responses in NOD mice are dominated by insulin epitope B:9-23 (InsB

Indexed as

Adoptive TransferAnimalsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Epitopes, T-LymphocyteForkhead Transcription FactorsInsulinMiceMice, Inbred NODMutationPeptide FragmentsReceptors, Antigen, T-CellT-LymphocytesT-Lymphocytes, RegulatoryEpitopes, T-LymphocyteForkhead Transcription FactorsFoxp3 protein, mouseInsulininsulin B (9-23)Peptide FragmentsReceptors, Antigen, T-Cell

Identifiers

PMID31836691
PMCPMC7034183
OpenAlexW2995153673

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.