Evidence map›Paper›PMID 29910814›Full record

ReviewFrontiers in immunology2018

The Role of Natural Killer Group 2, Member D in Chronic Inflammation and Autoimmunity.

Marina Babic, Chiara Romagnani

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 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

30 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
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  5. Review
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  7. Article
  8. Review
  9. Review
  10. Identification of small-molecule protein-protein interaction inhibitors for NKG2D.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Article
  12. [Role of CD4Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023
    Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Journal of personalized medicine · 2021
    Article
  19. Review
  20. 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

2 authors at 2 institutions in 1 country.

Marina BabicInnate Immunity, German Rheumatism Research Center (DRFZ), Leibniz Association, Berlin, Germany.
Chiara RomagnaniInnate Immunity, German Rheumatism Research Center (DRFZ), Leibniz Association, Berlin, Germany.
German Rheumatism Research Centre · DELeibniz Association · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current medicine and medical science puts great effort into elucidating the basis of chronicity and finding appropriate treatments for inflammatory diseases; however, the mechanisms driving aberrant immune responses are mostly unknown and deserve further study. Of particular interest is the identification of checkpoints that regulate the function and differentiation of pro-inflammatory cells during pathogenesis, along with means of their modulation for therapeutic purposes. Natural killer group 2, member D (NKG2D) is a potent activator of the immune system, known as a sensor for "induced-self" ligands, i.e., cellular danger signals that, in the context of chronic inflammation and autoimmunity, can be presented by cells being exposed to an inflammatory cytokine milieu, endoplasmic reticulum stress, or cell death. Engagement by such ligands can be translated by NKG2D into activation or co-stimulation of NK cells and different subsets of T cells, respectively, thus contributing to the regulation of the inflammatory response. In this review, we discuss the current knowledge on the contribution of the NKG2D-NKG2DL signaling axis during intestinal inflammation, type 1 diabetes, multiple sclerosis, and rheumatoid arthritis, where the role of NKG2D has been associated either by aberrant expression of the receptor and its ligands and/or by functional data in corresponding mouse models.

Indexed as

AnimalsAutoimmune DiseasesAutoimmunityChronic DiseaseDisease SusceptibilityGene Expression RegulationHumansInflammationLigandsNK Cell Lectin-Like Receptor Subfamily KSignal TransductionKLRK1 protein, humanLigandsNK Cell Lectin-Like Receptor Subfamily Kautoimmunityintestinal inflammationmember Dmember D ligandmultiple sclerosisnatural killer group 2rheumatoid arthritistype 1 diabetes

Identifiers

PMID29910814
PMCPMC5992374
OpenAlexW2803628848

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.