Evidence map›Paper›PMID 28704647›Full record

ArticleCell host & microbe2017

HIV-1-Mediated Downmodulation of HLA-C Impacts Target Cell Recognition and Antiviral Activity of NK Cells.

Christian Körner, Camille R Simoneau, Philipp Schommers, Mitchell Granoff, Maja Ziegler, Angelique Hölzemer, Sebastian Lunemann, Janet Chukwukelu, Björn Corleis, Vivek Naranbhai and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

33 citing papers in PubMed, 41 citations in OpenAlex.

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  12. Engaging innate immunity in HIV-1 cure strategies.Nature reviews. Immunology · 2022
    Review
  13. Review
  14. Frontiers in immunology · 2022
    Article
  15. Article
  16. Review
  17. Review
  18. Licensing Natural Killers for Antiviral Immunity.Pathogens (Basel, Switzerland) · 2021
    Review
  19. Article
  20. Article
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

16 authors at 6 institutions in 2 countries.

Christian KörnerHeinrich Pette Institute, Leibniz Institute for Experimental Virology, Department of Virus Immunology, 20251 Hamburg, Germany. Electronic address: christian.koerner@hpi.uni-hamburg.de.
Camille R SimoneauRagon Institute of MGH, MIT, and Harvard, Cambridge, MA 02139, USA.
Philipp SchommersHeinrich Pette Institute, Leibniz Institute for Experimental Virology, Department of Virus Immunology, 20251 Hamburg, Germany; Department I of Internal Medicine, University Hospital Cologne, 50937 Cologne, Germany; German Center for Infection Research (DZIF), Cologne, Germany.
Mitchell GranoffRagon Institute of MGH, MIT, and Harvard, Cambridge, MA 02139, USA.
Maja ZieglerHeinrich Pette Institute, Leibniz Institute for Experimental Virology, Department of Virus Immunology, 20251 Hamburg, Germany.
Angelique HölzemerHeinrich Pette Institute, Leibniz Institute for Experimental Virology, Department of Virus Immunology, 20251 Hamburg, Germany; German Center for Infection Research (DZIF), Hamburg, Germany; I. Department of Medicine, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Sebastian LunemannHeinrich Pette Institute, Leibniz Institute for Experimental Virology, Department of Virus Immunology, 20251 Hamburg, Germany.
Janet ChukwukeluHeinrich Pette Institute, Leibniz Institute for Experimental Virology, Department of Virus Immunology, 20251 Hamburg, Germany; German Center for Infection Research (DZIF), Hamburg, Germany.
Björn CorleisRagon Institute of MGH, MIT, and Harvard, Cambridge, MA 02139, USA.
Vivek NaranbhaiRagon Institute of MGH, MIT, and Harvard, Cambridge, MA 02139, USA; Cancer and Inflammation Program, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Douglas S KwonRagon Institute of MGH, MIT, and Harvard, Cambridge, MA 02139, USA; Division of Infectious Diseases, Massachusetts General Hospital, Boston, MA 02114, USA.
Eileen P ScullyRagon Institute of MGH, MIT, and Harvard, Cambridge, MA 02139, USA; Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Stephanie JostRagon Institute of MGH, MIT, and Harvard, Cambridge, MA 02139, USA; Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Boston, MA 02115, USA.
Frank KirchhoffInstitute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany.
Mary CarringtonRagon Institute of MGH, MIT, and Harvard, Cambridge, MA 02139, USA; Cancer and Inflammation Program, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, MD 21702, USA.
Marcus AltfeldHeinrich Pette Institute, Leibniz Institute for Experimental Virology, Department of Virus Immunology, 20251 Hamburg, Germany.
Leibniz Institute of Virology (LIV) · DERagon Institute of MGH, MIT and Harvard · USLeidos (United States) · USBeth Israel Deaconess Medical Center · USJohns Hopkins University · USUniversität Ulm · DE

Funding

Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STEVEN Grant DEEKS · 1988 to 2026
$93.6M
Effects of genetic polymorphism in MHC, KIR, and related loci on human diseaseZIABC010791 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI CARRINGTON, MARY N. · 2009 to 2025
$18.2M
NK cell mediated immune pressure in HIV-1 infectionR01AI067031 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI ALTFELD, MARCUS · 2006 to 2015
$4.4M
HIV-specific responses mediated by human NK cellsR01AI116363 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI JOST, STEPHANIE · 2015 to 2018
$1.7M
Harnessing NK cell activity to eliminate the HIV-1 reservoirK08AI116344 · NIAID · JOHNS HOPKINS UNIVERSITY · PI SCULLY, EILEEN PATRICIA · 2016 to 2020
$973k
CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001ENIAID NIH HHS K08 AI116344NIAID NIH HHS P30 AI027763NIAID NIH HHS R01 AI067031NIAID NIH HHS R01 AI116363
6 · The paper itself

Abstract

It was widely accepted that HIV-1 downregulates HLA-A/B to avoid CTL recognition while leaving HLA-C unaltered in order to prevent NK cell activation by engaging inhibitory NK cell receptors, but it was recently observed that most primary isolates of HIV-1 can mediate HLA-C downmodulation. Now we report that HIV-1-mediated downmodulation of HLA-C was associated with reduced binding to its respective inhibitory receptors. Despite this, HLA-C-licensed NK cells displayed reduced antiviral activity compared to their unlicensed counterparts, potentially due to residual binding to the respective inhibitory receptors. Nevertheless, NK cells were able to sense alterations of HLA-C expression demonstrated by increased antiviral activity when exposed to viral strains with differential abilities to downmodulate HLA-C. These results suggest that the capability of HLA-C-licensed NK cells to control HIV-1 replication is determined by the strength of KIR/HLA-C interactions and is thus dependent on both host genetics and the extent of virus-mediated HLA-C downregulation.

Indexed as

Antiviral AgentsCD4-Positive T-LymphocytesCell LineHEK293 CellsHIV-1HIV InfectionsHLA-A AntigensHLA-B AntigensHLA-C AntigensHumansKiller Cells, NaturalLymphocyte ActivationReceptors, KIR2DL1Receptors, KIR2DL3Virus ReplicationAntiviral AgentsHLA-A AntigensHLA-B AntigensHLA-C AntigensKIR2DL1 protein, humanKIR2DL3 protein, humanReceptors, KIR2DL1Receptors, KIR2DL3HIV-1HLA-CHLA class IKIRnatural killer cellsNK cells

Identifiers

PMID28704647
PMCPMC5565794
OpenAlexW2735576065

What OpenQuestion holds

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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.