Evidence map›Paper›PMID 25739961›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

NFκB activation by modified vaccinia virus as a novel strategy to enhance neutrophil migration and HIV-specific T-cell responses.

Mauro Di Pilato, Ernesto Mejías-Pérez, Manuela Zonca, Beatriz Perdiguero, Carmen Elena Gómez, Marianna Trakala, Jacobo Nieto, José Luis Nájera, Carlos Oscar S Sorzano, Christophe Combadière and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. 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
1.9field-weighted citation impact, top 14% 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, 32 citations in OpenAlex.

  1. Review
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  4. Neutrophils in oncolytic virus immunotherapy.Frontiers in immunology · 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

13 authors at 6 institutions in 4 countries.

Mauro Di PilatoDepartments of Molecular and Cellular Biology and.
Ernesto Mejías-PérezDepartments of Molecular and Cellular Biology and.
Manuela ZoncaImmunology and Oncology and.
Beatriz PerdigueroDepartments of Molecular and Cellular Biology and.
Carmen Elena GómezDepartments of Molecular and Cellular Biology and.
Marianna TrakalaCell Division and Cancer Group, Spanish National Cancer Research Centre, Madrid 28029, Spain;
Jacobo NietoDepartments of Molecular and Cellular Biology and.
José Luis NájeraDepartments of Molecular and Cellular Biology and.
Carlos Oscar S SorzanoBiocomputing Unit, Centro Nacional de Biotecnología/Consejo Superior de Investigaciones Cientificas, Madrid 28049, Spain;
Christophe CombadièreINSERM UMR_S 945, Faculté de Médecine Pitié-Salpétrière, Laboratoire Immunité et Infection, Paris 75013, France; and.
Giuseppe PantaleoDivision of Immunology and Allergy, Department of Medicine, Centre Hospitalier Universitaire Vaudois, University of Lausanne, Lausanne 1011, Switzerland.
Lourdes PlanellesImmunology and Oncology and.
Mariano EstebanDepartments of Molecular and Cellular Biology and mesteban@cnb.csic.es.
Bipar · FRConsejo Superior de Investigaciones Científicas · ESInserm · FRInstitute of Neuroimmunology of the Slovak Academy of Sciences · SKSpanish National Cancer Research Centre · ESUniversity of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils are antigen-transporting cells that generate vaccinia virus (VACV)-specific T-cell responses, yet how VACV modulates neutrophil recruitment and its significance in the immune response are unknown. We generated an attenuated VACV strain that expresses HIV-1 clade C antigens but lacks three specific viral genes (A52R, K7R, and B15R). We found that these genes act together to inhibit the NFκB signaling pathway. Triple ablation in modified virus restored NFκB function in macrophages. After virus infection of mice, NFκB pathway activation led to expression of several cytokines/chemokines that increased the migration of neutrophil populations (Nα and Nβ) to the infection site. Nβ cells displayed features of antigen-presenting cells and activated virus-specific CD8 T cells. Enhanced neutrophil trafficking to the infection site correlated with an increased T-cell response to HIV vector-delivered antigens. These results identify a mechanism for poxvirus-induced immune response and alternatives for vaccine vector design.

Indexed as

Immune System DiseasesLeukocyte DisordersAnimalsAntigen-Presenting CellsCD8-Positive T-LymphocytesCell LineGene DeletionGenes, ViralHIV-1HIV AntigensHumansLymphocyte ActivationMice, Inbred BALB CMice, Inbred C57BLModels, BiologicalNeutrophil InfiltrationHIV AntigensNF-kappa BHIVneutrophilsNFκBvaccinevaccinia virus

Identifiers

PMID25739961
PMCPMC4371968
OpenAlexW2137348686

What OpenQuestion holds

Textmetadata
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.