Evidence map›Paper›PMID 30166984›Full record

ReviewFrontiers in immunology2018

The Biological Influence and Clinical Relevance of Polymorphism Within the NKG2D Ligands.

Jianmin Zuo, Fiyaz Mohammed, Paul Moss

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. 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 23% 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, 22 citations in OpenAlex.

  1. Advances inFrontiers in immunology · 2026
    Article
  2. Association ofZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Article
  3. Article
  4. NKG2D-bispecific enhances NK and CD8+ T cell antitumor immunity.Cancer immunology, immunotherapy : CII · 2024
    Article
  5. Review
  6. Article
  7. Study of the association between aClinical and experimental hepatology · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. High-ThroughputFrontiers in immunology · 2020
    Article
  15. Review
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 1 institution in 1 country.

Jianmin ZuoInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
Fiyaz MohammedInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
Paul MossInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
University of Birmingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NKG2D is a major regulator of the activity of cytotoxic cells and interacts with eight different ligands (NKG2DL) from two families of MIC and ULBP proteins. The selective forces that drove evolution of NKG2DL are uncertain, but are likely to have been dominated by infectious disease and cancer. Of interest, NKG2DL are some of the most polymorphic genes outside the MHC locus and the study of these is uncovering a range of novel observations regarding the structure and function of NKG2DL. Polymorphism is present within all NKG2DL members and varies markedly within different populations. Allelic variation influences functional responses through three major mechanisms. First, it may drive differential levels of protein expression, modulate subcellular trafficking, or regulate release of soluble isoforms. In addition, it may alter the affinity of interaction with NKG2D or modulate cytotoxic activity from the target cell. In particular, ligands with high affinity for NKG2D are associated with down regulation of this protein on the effector cell, effectively limiting cytotoxic activity in a negative-feedback circuit. Given these observations, it is not surprising that NKG2DL alleles are associated with relative risk for development of several clinical disorders and the critical role of the NKG2D:NKG2DL interaction is demonstrated in many murine models. Increased understanding of the biophysical and functional consequences of this polymorphism is likely to provide insights into novel immunotherapeutic approaches.

Indexed as

Disease SusceptibilityPolymorphism, GeneticAnimalsClonal EvolutionClonal Selection, Antigen-MediatedCytotoxicity, ImmunologicHumansKiller Cells, NaturalLigandsNK Cell Lectin-Like Receptor Subfamily KProtein BindingSignal TransductionStructure-Activity RelationshipLigandsNK Cell Lectin-Like Receptor Subfamily Kbinding affinitycytotoxicityimmunologicnatural killer cellsNKG2D ligandspolymorphismsingle nucleotide

Identifiers

PMID30166984
PMCPMC6105697
OpenAlexW2887319658

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.