Evidence map›Paper›PMID 24146886›Full record

ArticlePloS one2013

High-throughput sequencing of islet-infiltrating memory CD4+ T cells reveals a similar pattern of TCR Vβ usage in prediabetic and diabetic NOD mice.

Idania Marrero, David E Hamm, Joanna D Davies

Abstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

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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

16 citing papers in PubMed.

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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

3 authors.

Idania MarreroTorrey Pines Institute for Molecular Studies, San Diego, California, United States of America.
David E Hamm
Joanna D Davies

Funding

B cell regulation of diabetogenic activityR01AI065937 · NIAID · TORREY PINES INST FOR MOLECULAR STUDIES · PI DAVIES, JOANNA D · 2007 to 2011
$2.2M
NIAID NIH HHS R01 AI065937NIAID NIH HHS R01AI065937
6 · The paper itself

Abstract

Autoreactive memory CD4(+) T cells play a critical role in the development of type 1 diabetes, but it is not yet known how the clonotypic composition and TCRβ repertoire of the memory CD4(+) T cell compartment changes during the transition from prediabetes to diabetes. In this study, we used high-throughput sequencing to analyze the TCRβ repertoire of sorted islet-infiltrating memory CD4(+)CD44(high) T cells in 10-week-old prediabetic and recently diabetic NOD mice. We show that most clonotypes of islet-infiltrating CD4(+)CD44(high) T cells were rare, but high-frequency clonotypes were significantly more common in diabetic than in prediabetic mice. Moreover, although the CD4(+)CD44(high) TCRβ repertoires were highly diverse at both stages of disease development, dominant use of TRBV1 (Vβ2), TRBV13-3 (Vβ8.1), and TRBV19 (Vβ6) was evident in both prediabetic and diabetic mice. Our findings strongly suggest that therapeutic targeting of cells specifically expressing the dominant TCRβ might reduce pancreatic infiltration in prediabetic mice and attenuate the progression to diabetes.

Indexed as

AnimalsBase SequenceCD4 AntigensCD4-Positive T-LymphocytesClone CellsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1FemaleGene Expression RegulationHigh-Throughput Nucleotide SequencingHyaluronan ReceptorsImmunologic MemoryIslets of LangerhansMiceMice, Inbred NODPrediabetic StateCD4 AntigensHyaluronan ReceptorsReceptors, Antigen, T-Cell, alpha-beta

Identifiers

PMID24146886
PMCPMC3798422

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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.