Evidence map›Paper›PMID 28445138›Full record

ArticleOncotarget2017

Killer cell immunoglobulin-like receptor 2DL4 is expressed in and suppresses the cell growth of Langerhans cell histiocytosis.

Yusuke Takei, Chiyuki Ueshima, Tatsuki R Kataoka, Masahiro Hirata, Akihiko Sugimoto, Mariyo Rokutan-Kurata, Koki Moriyoshi, Kazuo Ono, Ichiro Murakami, Sanju Iwamoto and 1 more

Open access · diamondAbstract read
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Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

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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

11 authors at 4 institutions in 1 country.

Yusuke TakeiDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Chiyuki UeshimaDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Tatsuki R KataokaDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Masahiro HirataDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Akihiko SugimotoDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Mariyo Rokutan-KurataDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Koki MoriyoshiDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Kazuo OnoDepartment of Pathology, Japan Red Cross Society Wakayama Medical Center, Wakayama, Japan.
Ichiro MurakamiDepartment of Pathology, School of Medicine, Kochi University Faculty of Medicine, Nankoku, Kochi, Japan.
Sanju IwamotoDepartment of Pharmacology, Toxicology & Therapeutics, Division of Physiology & Pathology, Showa University School of Pharmacy, Tokyo, Japan.
Hironori HagaDepartment of Diagnostic Pathology, Kyoto University Hospital, Kyoto, Japan.
Kyoto University Hospital · JPJapanese Red Cross Society Wakayama Medical Center · JPKōchi University · JPShowa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Killer cell immunoglobulin-like receptor (KIR) 2DL4 (CD158d) is a receptor for human leukocyte antigen-G. The function of KIR2DL4 has been reported in human natural killer cell lymphoma and mastocytosis, but not in Langerhans cell histiocytosis (LCH). Herein, we examined the expression and function of KIR2DL4 in LCHs. In pathological specimens, 27 of 36 LCH cases (75.0%) were immunohistochemically positive for KIR2DL4. Its expression was independent of age, gender, location, multi- or single-system, and the status of BRAFV600E immunostaining. We also confirmed the expression of KIR2DL4 mRNA and protein in the human LCH-like cell lines ELD-1 and PRU-1. KIR2DL4 protein was distributed in the membrane and cytoplasm of ELD-1 cells, but only in the cytoplasm of PRU-1 cells. An agonistic antibody against KIR2DL4 reduced phosphorylation of extracellular signal-regulated kinases (ERKs) and suppressed the cell growth of ELD-1 cells in a Src homology region 2 domain-containing phosphatase-2 dependent manner, but it had no effect in PRU-1 cells. These results suggest that KIR2DL4-mediated ERK suppression is a possible therapeutic target for LCH cells.

Indexed as

Gene ExpressionAdolescentAdultCell LineCell Line, TumorCell MembraneCell ProliferationChildChild, PreschoolCytoplasmExtracellular Signal-Regulated MAP KinasesFemaleHistiocytosis, Langerhans-CellHL-60 CellsHumansInfantExtracellular Signal-Regulated MAP KinasesReceptors, KIR2DL4ERKinhibitory receptorKIR2DL4Langerhans cell histiocytosisPathology SectionSHP-2

Identifiers

PMID28445138
PMCPMC5514884
OpenAlexW2605116551

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.