Evidence map›Paper›PMID 21076062›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

NKG2D is required for NK cell activation and function in response to E1-deleted adenovirus.

Jiangao Zhu, Xiaopei Huang, Yiping Yang

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. 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
1.2field-weighted citation impact, top 21% 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, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Human Adenovirus Associated Hepatic Injury.Frontiers in public health · 2022
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Natural killer cell responses to viral infection.Journal of innate immunity · 2011
    Review
  15. Article
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

3 authors at 2 institutions in 1 country.

Jiangao ZhuDepartment of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
Xiaopei Huang
Yiping Yang
Duke Medical Center · USDuke University Hospital · US

Funding

THERAPEUTIC APPROACHES TO OVARIAN/BREAST CANCER--HIGH DOSE CHEMOTHERAPY AND ABMSP01CA047741 · NCI · DUKE UNIVERSITY · PI HASSELBLAD, VICTOR · 1990 to 2013
$19.5M
Novel Strategies for Cancer Immunotherapy in Stem Cell TransplantR01CA136934 · NCI · OHIO STATE UNIVERSITY · PI YANG, YIPING · 2009 to 2018
$3.4M
Mechanisms for NK Cell Activation in Vaccinia Virus ControlU01AI083000 · NIAID · DUKE UNIVERSITY · PI YANG, YIPING · 2009 to 2013
$2.8M
NCI NIH HHS CA047741NCI NIH HHS CA136934NCI NIH HHS P01 CA047741NCI NIH HHS R01 CA136934NIAID NIH HHS AI083000NIAID NIH HHS U01 AI083000
6 · The paper itself

Abstract

Despite high transduction efficiency in vivo, the application of recombinant E1-deleted adenoviral vectors for in vivo gene therapy has been limited by the attendant innate and adaptive immune responses to adenoviral vectors. NK cells have been shown to play an important role in innate immune elimination of adenoviral vectors in vivo. However, the mechanisms underlying NK cell activation and function in response to adenoviral vectors remain largely undefined. In this study, we showed that NK cell activation upon adenoviral infection was dependent on accessory cells such as dendritic cells and macrophages and that cell contact-dependent signals from the accessory cells are necessary for NK cell activation. We further demonstrated that ligands of the NK activating receptor NKG2D were upregulated in accessory cells upon adenoviral infection and that blockade of NKG2D inhibited NK cell activation upon adenoviral infection, leading to a delay in adenoviral clearance in vivo. In addition, NKG2D was required for NK cell-mediated cytolysis on adenovirus-infected targets. Taken together, these results suggest that efficient NK cell activation and function in response to adenoviral infection is critically dependent on the NKG2D pathway, which understanding may assist in the design of effective strategies to improve the outcome of adenovirus-mediated gene therapy.

Indexed as

Adenovirus E1 ProteinsGene DeletionAdenoviridaeAdenoviridae InfectionsAnimalsDendritic CellsGenetic TherapyGenetic VectorsImmunity, InnateKiller Cells, NaturalLymphocyte ActivationMacrophagesMiceMice, KnockoutNK Cell Lectin-Like Receptor Subfamily KAdenovirus E1 ProteinsKlrk1 protein, mouseNK Cell Lectin-Like Receptor Subfamily K

Identifiers

PMID21076062
PMCPMC3008345
OpenAlexW2157407546

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.