Evidence map›Paper›PMID 37301761›Full record

ArticleJournal of the American Heart Association2023

Impact of NKG2D Signaling on Natural Killer and T-Cell Function in Cerebral Ischemia.

Christina David, Tobias Ruck, Leoni Rolfes, Stine Mencl, Peter Kraft, Michael K Schuhmann, Christina B Schroeter, Robin Jansen, Friederike Langhauser, Anne K Mausberg and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. CD8Nature reviews. Cardiology · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Highlighting a New Potential Target in Stroke: Immunoreceptor NKG2D.Journal of the American Heart Association · 2023
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Christina DavidDepartment of Neurology With Center for Translational Neuro- and Behavioral Sciences (C-TNBS) University Hospital Essen, University Duisburg-Essen Essen Germany.ORCID 0000-0001-5487-9979
Tobias RuckDepartment of Neurology, Medical Faculty Heinrich-Heine-University Düsseldorf Germany.ORCID 0000-0001-6332-8650
Leoni RolfesDepartment of Neurology, Medical Faculty Heinrich-Heine-University Düsseldorf Germany.
Stine MenclDepartment of Neurology With Center for Translational Neuro- and Behavioral Sciences (C-TNBS) University Hospital Essen, University Duisburg-Essen Essen Germany.
Peter KraftDepartment of Neurology Hospital Main-Spessart Lohr am Main Germany.
Michael K SchuhmannDepartment of Neurology University Hospital Würzburg Würzburg Germany.
Christina B SchroeterDepartment of Neurology, Medical Faculty Heinrich-Heine-University Düsseldorf Germany.
Robin JansenDepartment of Neurology, Medical Faculty Heinrich-Heine-University Düsseldorf Germany.
Friederike LanghauserDepartment of Neurology With Center for Translational Neuro- and Behavioral Sciences (C-TNBS) University Hospital Essen, University Duisburg-Essen Essen Germany.ORCID 0000-0002-6515-6191
Anne K MausbergDepartment of Neurology With Center for Translational Neuro- and Behavioral Sciences (C-TNBS) University Hospital Essen, University Duisburg-Essen Essen Germany.ORCID 0000-0001-9026-1703
Anke C FenderDepartment of Pharmacology University Hospital Essen, University of Duisburg-Essen Essen Germany.
Sven G MeuthDepartment of Neurology, Medical Faculty Heinrich-Heine-University Düsseldorf Germany.
Christoph KleinschnitzDepartment of Neurology With Center for Translational Neuro- and Behavioral Sciences (C-TNBS) University Hospital Essen, University Duisburg-Essen Essen Germany.ORCID 0000-0002-1650-8875
University of Duisburg-Essen · DEHeinrich Heine University Düsseldorf · DEUniversitätsklinikum Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background Typically defined as a thromboinflammatory disease, ischemic stroke features early and delayed inflammatory responses, which determine the extent of ischemia-related brain damage. T and natural killer cells have been implicated in neuronal cytotoxicity and inflammation, but the precise mechanisms of immune cell-mediated stroke progression remain poorly understood. The activating immunoreceptor NKG2D is expressed on both natural killer and T cells and may be critically involved. Methods and Results An anti-NKG2D blocking antibody alleviated stroke outcome in terms of infarct volume and functional deficits, coinciding with reduced immune cell infiltration into the brain and improved survival in the animal model of cerebral ischemia. Using transgenic knockout models devoid of certain immune cell types and immunodeficient mice supplemented with different immune cell subsets, we dissected the functional contribution of NKG2D signaling by different NKG2D-expressing cells in stroke pathophysiology. The observed effect of NKG2D signaling in stroke progression was shown to be predominantly mediated by natural killer and CD8

Indexed as

Brain IschemiaStrokeAnimalsCD8-Positive T-LymphocytesCerebral InfarctionHumansKiller Cells, NaturalMiceSignal Transductioninflammationmiddle cerebral artery occlusionnatural killer cellsNKG2D receptorstroke

Identifiers

PMID37301761
PMCPMC10356034
OpenAlexW4380204330

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.