Evidence map›Paper›PMID 22586038›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Type I IFN induced by adenovirus serotypes 28 and 35 has multiple effects on T cell immunogenicity.

Matthew J Johnson, Constantinos Petrovas, Takuya Yamamoto, Ross W B Lindsay, Karin Loré, Jason G D Gall, Emma Gostick, François Lefebvre, Mark J Cameron, David A Price and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 57 citations in OpenAlex.

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  5. Distinct Requirements for CD4European journal of immunology · 2025
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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

14 authors at 7 institutions in 4 countries.

Matthew J JohnsonImmunology Laboratory, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Constantinos Petrovas
Takuya Yamamoto
Ross W B Lindsay
Karin Loré
Jason G D Gall
Emma Gostick
François Lefebvre
Mark J Cameron
David A Price
Elias Haddad
Rafick-Pierre Sekaly
Robert A Seder
Richard A Koup
Vaccine & Gene Therapy Institute of Florida · USNational Institutes of Health · USInstitute of Infection and Immunity · CANational Institute of Allergy and Infectious Diseases · USGenVec · USGeorgetown University Medical Center · USKarolinska Institutet · SE

Funding

Optimization Of HIV Specific Immune Responses In VivoZIAAI005016 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SEDER, ROBERT A · 2009 to 2018
$31.2M
Tfh and B cells in HIV/SIV pathogenesis and vaccinationZIAAI005015 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KOUP, RICHARD A · 2009 to 2025
$24.1M
Testing of Blood Samples for Immune Response and Vaccine ResearchZIAAI005073 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KOUP, RICHARD A · 2009 to 2025
$23.4M
Intramural NIH HHS Z99 AI999999NIAID NIH HHS Y99 AI999999
6 · The paper itself

Abstract

Recombinant adenovirus (rAd) vectors are being investigated as vaccine delivery vehicles in preclinical and clinical studies. rAds constructed from different serotypes differ in receptor usage, tropism, and ability to activate cells, aspects of which likely contribute to their different immunogenicity profiles. In this study, we compared the infectivity and cell stimulatory capacity of recombinant adenovirus serotype 5 (rAd5), recombinant adenovirus serotype 28 (rAd28), and recombinant adenovirus serotype 35 (rAd35) in association with their respective immunogenicity profiles. We found that rAd28 and rAd35 infected and led to the in vitro maturation and activation of both human and mouse dendritic cells more efficiently compared with rAd5. In stark contrast to rAd5, rAd28 and rAd35 induced production of IFN-α and stimulated IFN-related intracellular pathways. However, the in vivo immunogenicity of rAd28 and rAd35 was significantly lower than that of rAd5. Deletion of IFN-α signaling during vaccination with rAd28 and rAd35 vectors increased the magnitude of the insert-specific T cell response to levels induced by vaccination with rAd5 vector. The negative impact of IFN-α signaling on the magnitude of the T cell response could be overcome by increasing the vaccine dose, which was also associated with greater polyfunctionality and a more favorable long-term memory phenotype of the CD8 T cell response in the presence of IFN-α signaling. Taken together, our results demonstrate that rAd-induced IFN-α production has multiple effects on T cell immunogenicity, the understanding of which should be considered in the design of rAd vaccine vectors.

Indexed as

AdenoviridaeAnimalsCell SeparationDendritic CellsFlow CytometryGene Expression ProfilingGenetic VectorsHumansInterferon Type IMiceMice, Inbred C57BLMicroarray AnalysisT-LymphocytesVaccines, SyntheticInterferon Type IVaccines, Synthetic

Identifiers

PMID22586038
PMCPMC3370104
OpenAlexW1942361731

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.