Evidence map›Paper›PMID 37741278›Full record

ArticleCell reports. Medicine2023

KLRG1 expression on natural killer cells is associated with HIV persistence, and its targeting promotes the reduction of the viral reservoir.

Antonio Astorga-Gamaza, David Perea, Nerea Sanchez-Gaona, Marta Calvet-Mirabent, Ana Gallego-Cortés, Judith Grau-Expósito, Ildefonso Sanchez-Cerrillo, Joan Rey, Josep Castellví, Adrian Curran and 7 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports. Medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

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  5. Resident CD49aScience advances · 2026
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  16. The role of KLRG1: a novel biomarker and new therapeutic target.Cell communication and signaling : CCS · 2024
    Review
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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

17 authors at 3 institutions in 1 country.

Antonio Astorga-GamazaInfectious Diseases Department, Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, 08035 Barcelona, Spain.
David PereaInfectious Diseases Department, Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, 08035 Barcelona, Spain.
Nerea Sanchez-GaonaInfectious Diseases Department, Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, 08035 Barcelona, Spain.
Marta Calvet-MirabentUniversidad Autónoma de Madrid, 28049 Madrid, Spain; Immunology Unit from Hospital Universitario de La Princesa and Instituto de Investigación Sanitaria Princesa, 28006 Madrid, Spain.
Ana Gallego-CortésInfectious Diseases Department, Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, 08035 Barcelona, Spain.
Judith Grau-ExpósitoInfectious Diseases Department, Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, 08035 Barcelona, Spain.
Ildefonso Sanchez-CerrilloUniversidad Autónoma de Madrid, 28049 Madrid, Spain; Immunology Unit from Hospital Universitario de La Princesa and Instituto de Investigación Sanitaria Princesa, 28006 Madrid, Spain.
Joan ReyInfectious Diseases Department, Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, 08035 Barcelona, Spain.
Josep CastellvíDepartment of Pathology, Hospital Vall d'Hebron, Universitat Autònoma de Barcelona, 08035 Barcelona, Spain.
Adrian CurranInfectious Diseases Department, Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, 08035 Barcelona, Spain.
Joaquin BurgosInfectious Diseases Department, Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, 08035 Barcelona, Spain.
Jordi NavarroInfectious Diseases Department, Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, 08035 Barcelona, Spain.
Paula SuanzesInfectious Diseases Department, Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, 08035 Barcelona, Spain.
Vicenç FalcóInfectious Diseases Department, Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, 08035 Barcelona, Spain.
Meritxell GenescàInfectious Diseases Department, Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, 08035 Barcelona, Spain.
Enrique Martín-GayoUniversidad Autónoma de Madrid, 28049 Madrid, Spain; Immunology Unit from Hospital Universitario de La Princesa and Instituto de Investigación Sanitaria Princesa, 28006 Madrid, Spain; Infectious Diseases CIBER (CIBERINFECC), Instituto de Salud Carlos III, 28029 Madrid, Spain.
Maria J BuzonInfectious Diseases Department, Hospital Universitari Vall d'Hebron, Institut de Recerca (VHIR), Universitat Autònoma de Barcelona, 08035 Barcelona, Spain. Electronic address: mariajose.buzon@vhir.org.
Universitat Autònoma de Barcelona · ESHospital Universitario de La Princesa · ESInstituto de Salud Carlos III · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human immunodeficiency virus (HIV) infection induces immunological dysfunction, which limits the elimination of HIV-infected cells during treated infection. Identifying and targeting dysfunctional immune cells might help accelerate the purging of the persistent viral reservoir. Here, we show that chronic HIV infection increases natural killer (NK) cell populations expressing the negative immune regulator KLRG1, both in peripheral blood and lymph nodes. Antiretroviral treatment (ART) does not reestablish these functionally impaired NK populations, and the expression of KLRG1 correlates with active HIV transcription. Targeting KLRG1 with specific antibodies significantly restores the capacity of NK cells to kill HIV-infected cells, reactivates latent HIV present in CD4

Indexed as

HIV-1HIV InfectionsReceptors, ImmunologicHumansKiller Cells, NaturalLectins, C-TypeVirus LatencyKLRG1 protein, humanLectins, C-TypeReceptors, ImmunologicHIV infectionHIV reservoirimmune checkpointimmunotherapyKLRG1natural killer

Identifiers

PMID37741278
PMCPMC10591043
OpenAlexW4386969544

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.