Evidence map›Paper›PMID 34115118›Full record

ArticleBlood2021

CMV exposure drives long-term CD57+ CD4 memory T-cell inflation following allogeneic stem cell transplant.

Albert C Yeh, Antiopi Varelias, Anupama Reddy, Sierra M Barone, Stuart D Olver, Kate Chilson, Lynn E Onstad, Kathleen S Ensbey, Andrea S Henden, Luke Samson and 11 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 8 institutions in 2 countries.

Albert C YehClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA.ORCID 0000-0003-3455-7360
Antiopi VareliasQIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.ORCID 0000-0002-3437-9659
Anupama ReddyPrism Bioanalytics, Durham, NC.
Sierra M BaroneDepartment of Cell and Developmental Biology, Vanderbilt University, Nashville, TN.
Stuart D OlverQIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Kate ChilsonClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA.
Lynn E OnstadClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA.
Kathleen S EnsbeyClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA.
Andrea S HendenQIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Luke SamsonClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA.
Carla A JaegerClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA.ORCID 0000-0002-1685-2078
Timothy BiVaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA.ORCID 0000-0002-5237-7024
Kimberly B DahlmanDivision of Hematology/Oncology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN; and.
Tae Kon KimDivision of Hematology/Oncology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN; and.
Ping ZhangClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA.
Mariapia A Degli-EspostiInfection and Immunity Program, Department of Microbiology, Biomedicine Discovery Institute, Monash University, Clayton, VIC, Australia.
Evan W NewellVaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA.
Madan H JagasiaDivision of Hematology/Oncology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN; and.
Jonathan M IrishDepartment of Cell and Developmental Biology, Vanderbilt University, Nashville, TN.ORCID 0000-0001-9428-8866
Stephanie J LeeClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA.ORCID 0000-0003-2600-6390
Geoffrey R HillClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA.
Fred Hutch Cancer Center · USQIMR Berghofer Medical Research Institute · AUUniversity of Washington Medical Center · USVanderbilt University Medical Center · USInfectious Disease Research Institute · USVanderbilt University · USAustralian Regenerative Medicine Institute · AUThe University of Queensland · AU

Funding

TRAINING IN CANCER BIOLOGY &TRANSPLANTATIONT32CA009515 · NCI · UNIVERSITY OF WASHINGTON · PI NANCY ELLEN DAVIDSON, Effie W Petersdorf · 1985 to 2026
$16.2M
Improving Outcomes Assessment in Chronic GVHDR01CA118953 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI LEE, STEPHANIE J · 2011 to 2025
$8.3M
Single Cell Methods for Bioeffector Discovery and AnalysisR01CA226833 · NCI · VANDERBILT UNIVERSITY · PI BRIAN O BACHMANN, Jonathan Michael Irish · 2019 to 2026
$6.1M
NCI NIH HHS R01 CA118953NCI NIH HHS R01 CA226833NCI NIH HHS T32 CA009515
6 · The paper itself

Abstract

Donor and recipient cytomegalovirus (CMV) serostatus correlate with transplant-related mortality that is associated with reduced survival following allogeneic stem cell transplant (SCT). Prior epidemiologic studies have suggested that CMV seronegative recipients (R-) receiving a CMV-seropositive graft (D+) experience inferior outcomes compared with other serostatus combinations, an observation that appears independent of viral reactivation. We therefore investigated the hypothesis that prior donor CMV exposure irreversibly modifies immunologic function after SCT. We identified a CD4+/CD57+/CD27- T-cell subset that was differentially expressed between D+ and D- transplants and validated results with 120 patient samples. This T-cell subset represents an average of 2.9% (D-/R-), 18% (D-/R+), 12% (D+/R-), and 19.6% (D+/R+) (P < .0001) of the total CD4+ T-cell compartment and stably persists for at least several years post-SCT. Even in the absence of CMV reactivation post-SCT, D+/R- transplants displayed a significant enrichment of these cells compared with D-/R- transplants (P = .0078). These are effector memory cells (CCR7-/CD45RA+/-) that express T-bet, Eomesodermin, granzyme B, secrete Th1 cytokines, and are enriched in CMV-specific T cells. These cells are associated with decreased T-cell receptor diversity (P < .0001) and reduced proportions of major histocompatibility class (MHC) II expressing classical monocytes (P < .0001), myeloid (P = .024), and plasmacytoid dendritic cells (P = .0014). These data describe a highly expanded CD4+ T-cell population and putative mechanisms by which prior donor or recipient CMV exposure may create a lasting immunologic imprint following SCT, providing a rationale for using D- grafts for R- transplant recipients.

Indexed as

CD4 AntigensCD4-Positive T-LymphocytesCD57 AntigensCells, CulturedCytomegalovirusCytomegalovirus InfectionsGraft vs Host DiseaseHematopoietic Stem Cell TransplantationHumansMemory T CellsTissue DonorsTransplantation, HomologousCD4 AntigensCD57 Antigens

Identifiers

PMID34115118
PMCPMC8718626
OpenAlexW3167232429

What OpenQuestion holds

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Registered trials

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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.