Evidence map›Paper›PMID 28468758›Full record

ArticleThe Journal of experimental medicine2017

Two alternate strategies for innate immunity to Epstein-Barr virus: One using NK cells and the other NK cells and γδ T cells.

Zakia Djaoud, Lisbeth A Guethlein, Amir Horowitz, Tarik Azzi, Neda Nemat-Gorgani, Daniel Olive, David Nadal, Paul J Norman, Christian Münz, Peter Parham

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 71 citations in OpenAlex.

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  7. When to suspect inborn errors of immunity in Epstein-Barr virus-related lymphoproliferative disorders.Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases · 2023
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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 4 institutions in 3 countries.

Zakia DjaoudDepartment of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305 zdjaoud@stanford.edu peropa@stanford.edu.ORCID 0000-0001-9583-8487
Lisbeth A GuethleinDepartment of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0002-1301-8301
Amir HorowitzDepartment of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305.
Tarik AzziExperimental Infectious Disease and Cancer Research, Children's Research Center, University Children's Hospital of Zurich, 8032 Zurich, Switzerland.ORCID 0000-0003-3490-2419
Neda Nemat-GorganiDepartment of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305.
Daniel OliveTeam Immunity and Cancer, Centre de Recherche en Cancérologie de Marseille (CRCM), Institut National de la Santé et de la Recherche Médicale, U1068; Centre National de la Recherche Scientifique, UMR7258, Institut Paoli-Calmettes; Aix-Marseille University, UM 105, 13284 Marseille, France.ORCID 0000-0003-1299-4113
David NadalExperimental Infectious Disease and Cancer Research, Children's Research Center, University Children's Hospital of Zurich, 8032 Zurich, Switzerland.ORCID 0000-0003-2712-1374
Paul J NormanDepartment of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305.ORCID 0000-0001-8370-7703
Christian MünzViral Immunobiology, Institute of Experimental Immunology, University of Zurich, 8006 Zurich, Switzerland.
Peter ParhamDepartment of Structural Biology, Stanford University School of Medicine, Stanford, CA 94305 zdjaoud@stanford.edu peropa@stanford.edu.
Stanford University · USUniversity Children's Hospital Zurich · CHAix-Marseille Université · FRUniversity of Zurich · CH

Funding

INTERACTIONS BETWEEN HLA CLASS I &CYTOLYTIC LYMPHOCYTESR01AI022039 · NIAID · STANFORD UNIVERSITY · PI PARHAM, PETER R · 1985 to 2017
$5.2M
CyTOFS10OD016318 · OD · STANFORD UNIVERSITY · PI NOLAN, GARRY P · 2013 to 2013
$600k
NIAID NIH HHS R01 AI022039NIH HHS S10 OD016318
6 · The paper itself

Abstract

Most humans become infected with Epstein-Barr virus (EBV), which then persists for life. Infrequently, EBV infection causes infectious mononucleosis (IM) or Burkitt lymphoma (BL). Type I EBV infection, particularly type I BL, stimulates strong responses of innate immune cells. Humans respond to EBV in two alternative ways. Of 24 individuals studied, 13 made strong NK and γδ T cell responses, whereas 11 made feeble γδ T cell responses but stronger NK cell responses. The difference does not correlate with sex, HLA type, or previous exposure to EBV or cytomegalovirus. Cohorts of EBV

Indexed as

Immunity, InnateAdultAntigens, CDB-LymphocytesButyrophilinsCell DifferentiationCell ProliferationCytomegalovirusEpstein-Barr Virus InfectionsGenotypeHerpesvirus 4, HumanHLA AntigensHumansKiller Cells, NaturalLymphocyte ActivationNK Cell Lectin-Like Receptor Subfamily KAntigens, CDBTN3A1 protein, humanButyrophilinsHLA AntigensKLRK1 protein, humanNK Cell Lectin-Like Receptor Subfamily KReceptors, Antigen, T-Cell, gamma-delta

Identifiers

PMID28468758
PMCPMC5460997
OpenAlexW2611617989

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.