Evidence map›Paper›PMID 26467237›Full record

ArticleEuropean journal of immunology2016

KIR2DL3 and KIR2DL1 show similar impact on licensing of human NK cells.

Malcolm J W Sim, Janet Stowell, Ruhena Sergeant, Daniel M Altmann, Eric O Long, Rosemary J Boyton

Open access · hybridAbstract read
In one paragraph

Article in European journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.7field-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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 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

6 authors at 2 institutions in 2 countries.

Malcolm J W SimLung Immunology Group, Infectious Diseases and Immunity, Department of Medicine, Imperial College London, Hammersmith Hospital, London, UK.
Janet StowellLung Immunology Group, Infectious Diseases and Immunity, Department of Medicine, Imperial College London, Hammersmith Hospital, London, UK.
Ruhena SergeantImperial College Healthcare NHS Trust, Hammersmith Hospital, London, UK.
Daniel M AltmannLung Immunology Group, Infectious Diseases and Immunity, Department of Medicine, Imperial College London, Hammersmith Hospital, London, UK.
Eric O LongLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA.
Rosemary J BoytonLung Immunology Group, Infectious Diseases and Immunity, Department of Medicine, Imperial College London, Hammersmith Hospital, London, UK.
Hammersmith Hospital · GBNational Institutes of Health · US

Funding

Regulation of immune responses by inhibitory receptorsZIAAI001117 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI LONG, ERIC O · 2009 to 2019
$5.7M
Wellcome Trust WT095472MA
6 · The paper itself

Abstract

Killer cell immunoglobulin-like receptor/HLA class I (KIR/HLA-I) combinations are associated with disease risk, implicating functional roles for NK cells (NKCs) or KIR(+) T cells. KIR/HLA-I interactions can act through inhibition of NKC activation by target cells and NKC licensing for greater intrinsic responsiveness. We compared licensing conferred by the weaker, HLA-C group 1/KIR2DL3, and the stronger, HLA-C group 2/KIR2DL1, inhibitory combinations. The "rheostat model" predicts weaker licensing by HLA-C1/KIR2DL3 interactions than HLA-C2/KIR2DL1. We analyzed degranulation in NKC subsets expressing single and multiple receptors for HLA-I. NKG2A had the strongest licensing impact, while KIR2DL3, KIR2DL1, and KIR3DL1 were weaker, and not significantly different to each other. Presence of one or two matched HLA-C allotypes did not alter licensing of KIR2DL3(+) and KIR2DL1(+) NKC. Coexpression of activating KIR2DS1 disarmed KIR2DL3(+) and KIR2DL1(+) NKC to a similar extent. KIR3DL1 and NKG2A combined for more enhanced licensing of double-positive NKC than the combination of KIR2DL3 and KIR2DL1. Thus, KIR2DL3 and KIR2DL1 have similar capacity to license NKC, suggesting that inhibitory signal strength and amount of available HLA-C ligands do not correlate with NKC licensing. Altogether, our results show that the basis for disease associations of HLA-C and KIR2DL likely encompasses factors other than licensing.

Indexed as

Flow CytometryHLA-C AntigensHumansKiller Cells, NaturalLymphocyte ActivationLymphocyte SubsetsReceptors, KIR2DL1Receptors, KIR2DL3HLA-C AntigensKIR2DL1 protein, humanKIR2DL3 protein, humanReceptors, KIR2DL1Receptors, KIR2DL3Human leukocyte antigen (HLA)Killer immunoglobulin-like receptor (KIR)LicensingNK cell (NKC)Rheostat model

Identifiers

PMID26467237
PMCPMC4737201
OpenAlexW1938480622

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.