Evidence map›Paper›PMID 33662046›Full record

ArticlePLoS pathogens2021

PD-1 is imprinted on cytomegalovirus-specific CD4+ T cells and attenuates Th1 cytokine production whilst maintaining cytotoxicity.

Helen M Parry, Alexander C Dowell, Jianmin Zuo, Kriti Verma, Francesca A M Kinsella, Jusnara Begum, Wayne Croft, Archana Sharma-Oates, Guy Pratt, Paul Moss

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  12. IL-10-Secreting CD8Pathogens (Basel, Switzerland) · 2022
    Article
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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

10 authors at 3 institutions in 1 country.

Helen M ParryInstitute of Immunology & Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.ORCID 0000-0002-9707-8167
Alexander C DowellInstitute of Immunology & Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.ORCID 0000-0002-1909-7047
Jianmin ZuoInstitute of Immunology & Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.ORCID 0000-0002-8341-465X
Kriti VermaInstitute of Immunology & Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.ORCID 0000-0002-7368-8171
Francesca A M KinsellaInstitute of Immunology & Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.ORCID 0000-0002-6022-2567
Jusnara BegumInstitute of Immunology & Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.ORCID 0000-0002-4230-3099
Wayne CroftInstitute of Immunology & Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.ORCID 0000-0001-6780-5944
Archana Sharma-OatesCentre for Computational Biology, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Guy PrattInstitute of Immunology & Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.
Paul MossInstitute of Immunology & Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham, United Kingdom.ORCID 0000-0002-6895-1967
University of Birmingham · GBGenomics (United Kingdom) · GBUniversity Hospitals Birmingham NHS Foundation Trust · GB

Funding

Cancer Research UK 29430Medical Research Council MR/R011230/1Wellcome Trust UNS29248
6 · The paper itself

Abstract

PD-1 is expressed on exhausted T cells in cancer patients but its physiological role remains uncertain. We determined the phenotype, function and transcriptional correlates of PD-1 expression on cytomegalovirus-specific CD4+ T cells during latent infection. PD-1 expression ranged from 10-85% and remained stable over time within individual donors. This 'setpoint' was correlated with viral load at primary infection. PD-1+ CD4+ T cells display strong cytotoxic function but generate low levels of Th1 cytokines which is only partially reversed by PD-1 blockade. TCR clonotypes showed variable sharing between PD-1+ and PD-1- CMV-specific cells indicating that PD-1 status is defined either during T cell priming or subsequent clonal expansion. Physiological PD-1+ CD4+ T cells therefore display a unique 'high cytotoxicity-low cytokine' phenotype and may act to suppress viral reactivation whilst minimizing tissue inflammation. Improved understanding of the physiological role of PD-1 will help to delineate the mechanisms, and potential reversal, of PD-1+ CD4+ T cell exhaustion in patients with malignant disease.

Indexed as

CD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCytokinesCytomegalovirusCytomegalovirus InfectionsGene ExpressionHumansProgrammed Cell Death 1 ReceptorViral LoadCytokinesProgrammed Cell Death 1 Receptor

Identifiers

PMID33662046
PMCPMC7963093
OpenAlexW3135868851

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.