Evidence map›Paper›PMID 26745675›Full record

ArticleOncotarget2016

Increased serum NKG2D-ligands and downregulation of NKG2D in peripheral blood NK cells of patients with major burns.

Josef Haik, Gil Nardini, Noga Goldman, Gilli Galore-Haskel, Moti Harats, Isaac Zilinsky, Oren Weissman, Jacob Schachter, Eyal Winkler, Gal Markel

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 33% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. High Activation of γδ T Cells and the γδ2Frontiers in immunology · 2019
    Article
  3. 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

10 authors at 2 institutions in 1 country.

Josef HaikDepartment of Plastic Surgery, Tel Aviv University, Tel Aviv, Israel.
Gil NardiniDepartment of Plastic Surgery, Tel Aviv University, Tel Aviv, Israel.
Noga GoldmanDepartment of General Surgery C, Tel Aviv University, Tel Aviv, Israel.
Gilli Galore-HaskelElla Institute of Melanoma, Sheba Medical Center, Ramat Gan, Israel.
Moti HaratsDepartment of Plastic Surgery, Tel Aviv University, Tel Aviv, Israel.
Isaac ZilinskyDepartment of Plastic Surgery, Tel Aviv University, Tel Aviv, Israel.
Oren WeissmanDepartment of Plastic Surgery, Tel Aviv University, Tel Aviv, Israel.
Jacob SchachterSackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Eyal WinklerDepartment of Plastic Surgery, Tel Aviv University, Tel Aviv, Israel.
Gal MarkelTalpiot Medical Leadership Program, Tel Aviv University, Tel Aviv, Israel.
Tel Aviv University · ILSheba Medical Center · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune suppression following major thermal injury directly impacts the recovery potential. Limited data from past reports indicate that natural killer cells might be suppressed due to a putative soluble factor that has remained elusive up to date. Here we comparatively study cohorts of patients with Major and Non-Major Burns as well as healthy donors. MICB and ULBP1 are stress ligands of NKG2D that can be induced by heat stress. Remarkably, serum concentration levels of MICB and ULBP1 are increased by 3-fold and 20-fold, respectively, already within 24h post major thermal injury, and are maintained high for 28 days. In contrast, milder thermal injuries do not similarly enhance the serum levels of MICB and ULBP1. This kinetics coincides with a significant downregulation of NKG2D expression among peripheral blood NK cells. Downregulation of NKG2D by high concentration of soluble MICB occurs in cancer patients and during normal pregnancy due to over production by cancer cells or extravillous trophoblasts, respectively, as an active immune-evasion mechanism. In burn patients this seems an incidental outcome of extensive thermal injury, leading to reduced NKG2D expression. Enhanced susceptibility of these patients to opportunistic viral infections, particularly herpes viruses, could be explained by the reduced NKG2D expression. Further studies are warranted for translation into innovative diagnostic or therapeutic technologies.

Indexed as

AdultBurnsFemaleGPI-Linked ProteinsHistocompatibility Antigens Class IHumansIntracellular Signaling Peptides and ProteinsKiller Cells, NaturalMaleMiddle AgedNeoplasmsNK Cell Lectin-Like Receptor Subfamily KOpportunistic InfectionsYoung AdultGPI-Linked ProteinsHistocompatibility Antigens Class IIntracellular Signaling Peptides and ProteinsKLRK1 protein, humanMICB antigenNK Cell Lectin-Like Receptor Subfamily KULBP1 protein, humanburnsImmune responseimmune suppressionImmunityImmunology and Microbiology Sectionlysis receptorsMICBnatural killer

Identifiers

PMID26745675
PMCPMC4823030
OpenAlexW2203944690

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.