Evidence map›Paper›PMID 32526772›Full record

ArticleThe Journal of experimental medicine2020

Poor quality Vβ recombination signal sequences stochastically enforce TCRβ allelic exclusion.

Glendon S Wu, Katherine S Yang-Iott, Morgann A Klink, Katharina E Hayer, Kyutae D Lee, Craig H Bassing

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

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  17. Inefficient V(D)J recombination underlies monogenic T cell receptor β expression.Proceedings of the National Academy of Sciences of the United States of America · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Glendon S WuImmunology Graduate Group, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Katherine S Yang-IottDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Morgann A KlinkDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Katharina E HayerDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Kyutae D LeeDepartment of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Craig H BassingImmunology Graduate Group, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Children's Hospital of Philadelphia · US

Funding

Immune System Development and RegulationT32AI055428 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI ALLMAN, DAVID M, OLIVER, PAULA MARIA · 2003 to 2025
$4.2M
Topological Control of Antigen Receptor Loci during Lymphocyte DevelopmentR01AI130231 · NIAID · CHILDREN'S HOSP OF PHILADELPHIA · PI BASSING, CRAIG H, OLTZ, EUGENE M · 2017 to 2021
$3.8M
Elucidating Lymphocyte Allelic Exclusion Mechanisms and FunctionsR01AI143661 · NIAID · CHILDREN'S HOSP OF PHILADELPHIA · PI BASSING, CRAIG H · 2019 to 2023
$2.2M
NIAID NIH HHS R01 AI130231NIAID NIH HHS R01 AI143661NIAID NIH HHS T32 AI055428
6 · The paper itself

Abstract

The monoallelic expression of antigen receptor (AgR) genes, called allelic exclusion, is fundamental for highly specific immune responses to pathogens. This cardinal feature of adaptive immunity is achieved by the assembly of a functional AgR gene on one allele, with subsequent feedback inhibition of V(D)J recombination on the other allele. A range of epigenetic mechanisms have been implicated in sequential recombination of AgR alleles; however, we now demonstrate that a genetic mechanism controls this process for Tcrb. Replacement of V(D)J recombinase targets at two different mouse Vβ gene segments with a higher quality target elevates Vβ rearrangement frequency before feedback inhibition, dramatically increasing the frequency of T cells with TCRβ chains derived from both Tcrb alleles. Thus, TCRβ allelic exclusion is enforced genetically by the low quality of Vβ recombinase targets that stochastically restrict the production of two functional rearrangements before feedback inhibition silences one allele.

Indexed as

AllelesProtein Sorting SignalsAnimalsBase SequenceFeedback, PhysiologicalGene Expression RegulationHybridomasMice, Inbred C57BLMice, TransgenicProtein BindingProto-Oncogene Proteins c-fosReceptors, Antigen, T-Cell, alpha-betaThymocytesT-LymphocytesV(D)J RecombinationProtein Sorting SignalsProto-Oncogene Proteins c-fosReceptors, Antigen, T-Cell, alpha-beta

Identifiers

PMID32526772
PMCPMC7478721
OpenAlexW3034631588

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.