Evidence map›Paper›PMID 26720279›Full record

ArticlePLoS pathogens2015

Dual Requirement of Cytokine and Activation Receptor Triggering for Cytotoxic Control of Murine Cytomegalovirus by NK Cells.

Bijal A Parikh, Sytse J Piersma, Melissa A Pak-Wittel, Liping Yang, Robert D Schreiber, Wayne M Yokoyama

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 48 citations in OpenAlex.

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  14. Licensing Natural Killers for Antiviral Immunity.Pathogens (Basel, Switzerland) · 2021
    Review
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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

6 authors at 1 institution in 1 country.

Bijal A ParikhDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Sytse J PiersmaDivision of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Melissa A Pak-WittelDivision of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Liping YangDivision of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Robert D SchreiberDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Wayne M YokoyamaDivision of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Washington University in St. Louis · US

Funding

Viral Discovery in Rheumatoid ArthritisP30AR048335 · NIAMS · WASHINGTON UNIVERSITY · PI BYUN, MINJI · 2001 to 2015
$8.9M
Specificity of Murine CMV Resistance by NK CellsR01AI051345 · NIAID · WASHINGTON UNIVERSITY · PI YOKOYAMA, WAYNE M. · 2002 to 2016
$4.5M
DEVELOPMENT OF GENOMICS BASED PERSONALIZED CANCER IMMUNOTHERAPYR01CA190700 · NCI · WASHINGTON UNIVERSITY · PI SCHREIBER, ROBERT DAVID · 2015 to 2019
$2.1M
MECHANISMS OF THE NATURAL KILLER CELL ANTIVIRAL EFFECTOR RESPONSEK08AI104991 · NIAID · WASHINGTON UNIVERSITY · PI PARIKH, BIJAL A. · 2013 to 2017
$844k
NIAID NIH HHS K08 AI104991NIAID NIH HHS K08-AI104991NIAID NIH HHS R01 AI051345NIAID NIH HHS R01-AI051345NIAMS NIH HHS P30 AR048335NIAMS NIH HHS P30-AR048335
6 · The paper itself

Abstract

Natural killer (NK) cells play a critical role in controlling murine cytomegalovirus (MCMV) and can mediate both cytokine production and direct cytotoxicity. The NK cell activation receptor, Ly49H, is responsible for genetic resistance to MCMV in C57BL/6 mice. Recognition of the viral m157 protein by Ly49H is sufficient for effective control of MCMV infection. Additionally, during the host response to infection, distinct immune and non-immune cells elaborate a variety of pleiotropic cytokines which have the potential to impact viral pathogenesis, NK cells, and other immune functions, both directly and indirectly. While the effects of various immune deficiencies have been examined for general antiviral phenotypes, their direct effects on Ly49H-dependent MCMV control are poorly understood. To specifically interrogate Ly49H-dependent functions, herein we employed an in vivo viral competition approach to show Ly49H-dependent MCMV control is specifically mediated through cytotoxicity but not IFNγ production. Whereas m157 induced Ly49H-dependent degranulation, efficient cytotoxicity also required either IL-12 or type I interferon (IFN-I) which acted directly on NK cells to produce granzyme B. These studies demonstrate that both of these distinct NK cell-intrinsic mechanisms are integrated for optimal viral control by NK cells.

Indexed as

AnimalsCytokinesCytotoxicity, ImmunologicFlow CytometryHerpesviridae InfectionsKiller Cells, NaturalLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutMuromegalovirusNK Cell Lectin-Like Receptor Subfamily ASignal TransductionCytokinesKlra8 protein, mouseNK Cell Lectin-Like Receptor Subfamily A

Identifiers

PMID26720279
PMCPMC4697817
OpenAlexW2202901642

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.