Evidence map›Paper›PMID 24440149›Full record

ArticleImmunity2014

Costimulatory molecule DNAM-1 is essential for optimal differentiation of memory natural killer cells during mouse cytomegalovirus infection.

Tsukasa Nabekura, Minoru Kanaya, Akira Shibuya, Guo Fu, Nicholas R J Gascoigne, Lewis L Lanier

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed
10.1field-weighted citation impact, top 1% 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

109 citing papers in PubMed, 181 citations in OpenAlex.

  1. Trial
  2. Article
  3. Therapeutic bacteria-trained NK cells confer long-term protection against cancer metastasis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
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  11. Immunological Profiling of CD8International journal of molecular sciences · 2024
    Article
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  17. Article
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49 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Tsukasa NabekuraDepartment of Microbiology and Immunology and the Cancer Research Institute, University of California, San Francisco, San Francisco, CA 94143, USA.
Minoru KanayaDepartment of Immunology, Division of Biomedical Sciences, University of Tsukuba, Ibaraki 305-8575, Japan.
Akira ShibuyaDepartment of Immunology, Division of Biomedical Sciences, University of Tsukuba, Ibaraki 305-8575, Japan.
Guo FuDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.
Nicholas R J GascoigneDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.
Lewis L LanierDepartment of Microbiology and Immunology and the Cancer Research Institute, University of California, San Francisco, San Francisco, CA 94143, USA. Electronic address: lewis.lanier@ucsf.edu.
Cancer Research Institute · USScripps Research Institute · USUniversity of Tsukuba · JP

Funding

Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STEVEN Grant DEEKS · 1988 to 2026
$93.6M
UCSF Liver Core CenterP30DK026743 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Holger Willenbring · 1986 to 2026
$30.7M
NK MemoryR01AI068129 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LANIER, LEWIS LEE · 2006 to 2020
$6.0M
Intermolecular Interactions in the Immunological SynapseR01GM065230 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI SAUER, KARSTEN · 2002 to 2014
$4.6M
Mechanisms of effective innate immunity in HCV treatmentU19AI088790 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RYAN, JAMES C · 2010 to 2014
$3.6M
NIAID NIH HHS AI068129NIAID NIH HHS P30 AI027763NIAID NIH HHS R01 AI068129NIAID NIH HHS U19 AI088790NIDDK NIH HHS P30 DK026743NIGMS NIH HHS GM065230NIGMS NIH HHS R01 GM065230
6 · The paper itself

Abstract

Recent studies demonstrate that natural killer (NK) cells have adaptive immune features. Here, we investigated the role of the costimulatory molecule DNAM-1 in the differentiation of NK cells in a mouse model of cytomegalovirus (MCMV) infection. Antibody blockade of DNAM-1 suppressed the expansion of MCMV-specific Ly49H(+) cells during viral infection and inhibited the generation of memory NK cells. Similarly, DNAM-1-deficient (Cd226(-/-)) Ly49H(+) NK cells exhibited intrinsic defects in expansion and differentiation into memory cells. Src-family tyrosine kinase Fyn and serine-threonine protein kinase C isoform eta (PKCη) signaling through DNAM-1 played distinct roles in the generation of MCMV-specific effector and memory NK cells. Thus, cooperative signaling through DNAM-1 and Ly49H are required for NK cell-mediated host defense against MCMV infection.

Indexed as

Cell DifferentiationAnimalsAntigens, Differentiation, T-LymphocyteCytomegalovirus InfectionsDisease Models, AnimalImmunity, InnateKiller Cells, NaturalMiceMice, Inbred C57BLMuromegalovirusT Lineage-Specific Activation Antigen 1Antigens, Differentiation, T-LymphocyteT Lineage-Specific Activation Antigen 1

Identifiers

PMID24440149
PMCPMC3943894
OpenAlexW2060798773

What OpenQuestion holds

Textmetadata
LicenceTDM
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.