Evidence map›Paper›PMID 23756244›Full record

ReviewCritical reviews in immunology2013

The yin-yang of KIR3DL1/S1: molecular mechanisms and cellular function.

Geraldine M O'Connor, Daniel McVicar

Open access · greenAbstract readReview
In one paragraph

Review in Critical reviews in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  3. Impact ofFrontiers in cellular and infection microbiology · 2026
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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

2 authors at 1 institution in 2 countries.

Geraldine M O'ConnorCancer and Inflammation Program, National Cancer Institute at Frederick, NIH, Frederick, MD 21702, USA.
Daniel McVicar
Frederick National Laboratory for Cancer Research · US

Funding

Charaterization of the Expression and Ligands of KIR3DS1ZIABC010747 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MCVICAR, DANIEL W. · 2009 to 2018
$1.8M
Charaterization of the Expression and Ligands of KIR3DS1Z01BC010747 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI MCVICAR, DANIEL W. · 2006 to 2008
$346k
Intramural NIH HHS Z01 BC010747
6 · The paper itself

Abstract

Killer Immunoglobulin-like Receptors (KIR) are a family of receptors expressed on natural killer (NK) and T-cell subsets. KIR3DL1 is a highly polymorphic receptor that binds to groups of HLAA and HLA-B allotypes that express the Bw4 epitope. The variation in KIR3DL1 allotypes manifests at a number of levels. Most dramatically, a common allelic variant encodes an activating rather than an inhibitory receptor (KIR3DS1). In addition, sequence variants can affect both the frequency of expression within the NK cell population and the intensity of expression on a given cell. KIR3DL1 polymorphism also influences the interaction with HLA-Bw4 molecules, due to contacts with the HLA molecule itself and sensitivity to the presented peptide. A body of evidence from genetic association studies supports the biological significance not only of the interaction of KIR3DL1 with HLA-Bw4 but also the functional variation seen with different KIR3DL1 and HLA allotypes. In this review, we discuss our current understanding of KIR3DL1 function and our recent insights from the structure of the KIR3DL1 in complex with HLA. In addition, we will summarize our current understanding of KIR3DS1, including its ligand specificity and its role in immune responses.

Indexed as

Gene Expression RegulationHistocompatibility Antigens Class IHumansLigandsPolymorphism, GeneticProtein BindingReceptors, KIR3DL1Histocompatibility Antigens Class ILigandsReceptors, KIR3DL1

Identifiers

PMID23756244
PMCPMC3741655
OpenAlexW2079355254

What OpenQuestion holds

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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.