Evidence map›Paper›PMID 21115737›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Interactions of NK cell receptor KIR3DL1*004 with chaperones and conformation-specific antibody reveal a functional folded state as well as predominant intracellular retention.

Sabrina B Taner, Marcelo J Pando, Allison Roberts, Jennifer Schellekens, Steven G E Marsh, Karl-Johan Malmberg, Peter Parham, Frances M Brodsky

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

27 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
  2. Article
  3. A New GlyT2 Variant Associated with Hyperekplexia.International journal of molecular sciences · 2025
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  15. Article
  16. KIR3DL1/HLA-B Subtypes Govern Acute Myelogenous Leukemia Relapse After Hematopoietic Cell Transplantation.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2017
    Article
  17. KIR3DL1 Allelic Polymorphism and HLA-B Epitopes Modulate Response to Anti-GD2 Monoclonal Antibody in Patients With Neuroblastoma.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2016
    Article
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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

8 authors at 5 institutions in 3 countries.

Sabrina B TanerDepartment of Bioengineering and Therapeutic Sciences, University of California, San Francisco, San Francisco, CA 94143, USA.
Marcelo J Pando
Allison Roberts
Jennifer Schellekens
Steven G E Marsh
Karl-Johan Malmberg
Peter Parham
Frances M Brodsky
University of California, San Francisco · USAnthony Nolan · GBKarolinska Institutet · SEStanford University · USUniversity of San Francisco · US

Funding

NK Cells and HIV InfectionP01AI064520 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BRODSKY, FRANCES M. · 2005 to 2009
$6.2M
INTERACTIONS BETWEEN HLA CLASS I &CYTOLYTIC LYMPHOCYTESR01AI022039 · NIAID · STANFORD UNIVERSITY · PI PARHAM, PETER R · 1985 to 2017
$5.2M
THE MOLECULAR MECHANISM OF CLATHRIN ASSEMBLYR01GM038093 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BRODSKY, FRANCES M. · 1988 to 2014
$5.0M
NIAID NIH HHS P01 AI064520NIAID NIH HHS R01 AI022039NIGMS NIH HHS R01 GM038093
6 · The paper itself

Abstract

Variable interaction between the Bw4 epitope of HLA-B and the polymorphic KIR3DL1/S1 system of inhibitory and activating NK cell receptors diversifies the development, repertoire formation, and response of human NK cells. KIR3DL1*004, a common KIR3DL1 allotype, in combination with Bw4(+) HLA-B, slows progression of HIV infection to AIDS. Analysis in this study of KIR3DL1*004 membrane traffic in NK cells shows this allotype is largely misfolded but stably retained in the endoplasmic reticulum, where it binds to the chaperone calreticulin and does not induce the unfolded protein response. A small fraction of KIR3DL1*004 folds correctly and leaves the endoplasmic reticulum to be expressed on the surface of primary NK and transfected NKL cells, in a form that can be triggered to inhibit NK cell activation and secretion of IFN-γ. Consistent with this small proportion of correctly folded molecules, trace amounts of MHC class I coimmunoprecipitated with KIR3DL1*004. There was no indication of any extensive intracellular interaction between unfolded KIR3DL1*004 and cognate Bw4(+) HLA-B. A similarly limited interaction of Bw4 with KIR3DL1*002, when both were expressed by the same cell, was observed despite the efficient folding of KIR3DL1*002 and its abundance on the NK cell surface. Several positions of polymorphism modulate KIR3DL1 abundance at the cell surface, differences that do not necessarily correlate with the potency of allotype function. In this context, our results suggest the possibility that the effect of Bw4(+) HLA-B and KIR3DL1*004 in slowing progression to AIDS is mediated by interaction of Bw4(+) HLA-B with the small fraction of cell surface KIR3DL1*004.

Indexed as

Protein FoldingAntibodies, MonoclonalCalreticulinCell LineEndoplasmic ReticulumHLA-B AntigensHumansIntracellular FluidKiller Cells, NaturalLigandsMolecular ChaperonesProtein BindingProtein ConformationProtein TransportProtein UnfoldingReceptors, KIR3DL1Antibodies, MonoclonalCalreticulinHLA-B AntigensHLA-Bw4 antigenKIR3DL1 protein, humanLigandsMolecular ChaperonesReceptors, KIR3DL1

Identifiers

PMID21115737
PMCPMC3129036
OpenAlexW2151851630

What OpenQuestion holds

Textmetadata
LicenceTDM
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.