Evidence map›Paper›PMID 27183386›Full record

ArticleThe Journal of clinical investigation2016

A "hotspot" for autoimmune T cells in type 1 diabetes.

Brian D Stadinski, Reinhard Obst, Eric S Huseby

Abstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Brian D Stadinski
Reinhard Obst
Eric S Huseby

Funding

T cell and transgenic core U19AI109858 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HUSEBY, ERIC S · 2014 to 2018
$11.9M
TRAINING IN IMMUNOLOGY (COMPETITIVE RENEWAL OF AI07439)T32AI007349 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI STERN, LAWRENCE J. · 1989 to 2024
$4.5M
Origin and Control of Self-Reactive TCRsR01DK095077 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HUSEBY, ERIC S · 2012 to 2016
$1.8M
Biotechnology and Biological Sciences Research Council BB/H001085/1NIAID NIH HHS T32 AI007349NIAID NIH HHS U19 AI109858NIDDK NIH HHS R01 DK095077
6 · The paper itself

Abstract

The ability of a single T cell antigen receptor (TCR) to cross-react with multiple antigens allows the finite number of T cells within an organism to respond to the compendium of pathogen challenges faced during a lifetime. Effective immune surveillance, however, comes at a price. TCR cross-reactivity can allow molecular mimics to spuriously activate autoimmune T cells; it also underlies T cell rejection of organ transplants and drives graft-versus-host disease. In this issue of the JCI, Cole and colleagues provide insight into how an insulin-reactive T cell cross-reacts with pathogen-derived antigens by focusing on a limited portion of the peptides to provide a hotspot for binding. These findings dovetail with recent studies of alloreactive and autoimmune TCRs and suggest that the biochemical principles that govern conventional protein-protein interactions may allow the specificity and cross-reactivity profiles of T cells to be predicted.

Indexed as

Diabetes Mellitus, Type 1Graft vs Host DiseaseHumansPeptidesReceptors, Antigen, T-CellT-LymphocytesPeptidesReceptors, Antigen, T-Cell

Identifiers

PMID27183386
PMCPMC4887178

What OpenQuestion holds

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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.