Evidence map›Paper›PMID 26080707›Full record

ArticleMucosal immunology2016

Dynamic change in natural killer cell type in the human ocular mucosa in situ as means of immune evasion by adenovirus infection.

N Yawata, K J Selva, Y-C Liu, K P Tan, A W L Lee, J Siak, W Lan, M Vania, A Arundhati, L Tong and 3 more

Open access · bronzeAbstract read
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In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

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  5. Evaluation ofFrontiers in bioengineering and biotechnology · 2025
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  6. Review
  7. [Flow cytometry analysis of normal range of natural killer cells and their subsets in peripheral blood of healthy Chinese adults].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2024
    Article
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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

13 authors at 6 institutions in 2 countries.

N YawataSingapore Eye Research Institute, Singapore, Singapore.
K J SelvaSingapore Eye Research Institute, Singapore, Singapore.
Y-C LiuSingapore Eye Research Institute, Singapore, Singapore.
K P TanSingapore Institute for Clinical Sciences (SICS), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
A W L LeeSingapore Institute for Clinical Sciences (SICS), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
J SiakSingapore Eye Research Institute, Singapore, Singapore.
W LanSingapore Eye Research Institute, Singapore, Singapore.
M VaniaSingapore Eye Research Institute, Singapore, Singapore.
A ArundhatiSingapore National Eye Centre, Singapore, Singapore.
L TongSingapore Eye Research Institute, Singapore, Singapore.
J LiXinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
J S MehtaSingapore Eye Research Institute, Singapore, Singapore.
M YawataSingapore Institute for Clinical Sciences (SICS), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Singapore Eye Research Institute · SGSingapore Institute for Clinical Sciences · SGSingapore National Eye Center · SGNational University Health System · SGNational University of Singapore · SGShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The most severe form of virus-induced inflammation at the ocular surface is epidemic keratoconjunctivitis (EKC), often caused by group D human adenoviruses (HAdVs). We investigated the dynamics and mechanisms of changes in natural killer (NK) cell types in the human ocular mucosal surface in situ over the course of infection. In the acute phase of infection, the mature CD56(dim)NK cells that comprise a major subpopulation in the normal human conjunctiva are replaced by CD56(bright)NK cells recruited to the ocular surface by chemokines produced by the infected epithelium, and NKG2A-expressing CD56(dim) and CD56(bright) NK cells become the major subpopulations in severe inflammation. These NK cells attracted to the mucosal surface are however incapable of mounting a strong antiviral response because of upregulation of the inhibitory ligand human leukocyte antigen-E (HLA-E) on infected epithelium. Furthermore, group D HAdVs downregulate ligands for activating NK cell receptors, thus rendering even the mature NKG2A(-)NK cells unresponsive, an immune-escape mechanism distinct from other adenoviruses. Our findings imply that the EKC-causing group D HAdVs utilize these multiple pathways to inhibit antiviral NK cell responses in the initial stages of the infection.

Indexed as

Immune EvasionAdenoviridaeAdenoviridae InfectionsCD56 AntigenCell Line, TumorChemokinesChemotaxisCoculture TechniquesConjunctivaConjunctivitis, ViralEpithelial CellsGene Expression RegulationHistocompatibility Antigens Class IHLA-E AntigensHumansKiller Cells, NaturalCD56 AntigenChemokinesHistocompatibility Antigens Class IHLA-E AntigensKLRC1 protein, humanNCAM1 protein, humanNK Cell Lectin-Like Receptor Subfamily C

Identifiers

PMID26080707
OpenAlexW1493677120

What OpenQuestion holds

Textmetadata
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.