Evidence map›Paper›PMID 22902724›Full record

ArticleJournal of acquired immune deficiency syndromes (1999)2012

Plasma factors during chronic HIV-1 infection impair IL-12 secretion by myeloid dendritic cells via a virus-independent pathway.

Elizabeth A Miller, Meredith R Spadaccia, Meagan P OʼBrien, Linda Rolnitzky, Rachel Sabado, Olivier Manches, Davor Frleta, Nina Bhardwaj

Abstract read
In one paragraph

Article in Journal of acquired immune deficiency syndromes (1999), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

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  16. Advances in dendritic cell immunotherapies for HIV-1 infection.Expert opinion on biological therapy · 2014
    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

8 authors at 1 institution in 1 country.

Elizabeth A MillerDepartment of Medicine, New York University School of Medicine, New York, NY 10016, USA.
Meredith R Spadaccia
Meagan P OʼBrien
Linda Rolnitzky
Rachel Sabado
Olivier Manches
Davor Frleta
Nina Bhardwaj
New York University · US

Funding

Viral and Host Determinants of HIV-1 TransmissionU01AI067854 · NIAID · DUKE UNIVERSITY · PI HAYNES, BARTON F · 2005 to 2005
$14.9M
Thymic output, lymphocyte activation and turnoverP01AI057127 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI VALENTINE, FRED T · 2004 to 2009
$9.0M
Modulating anti-HIV immunity by plasmacytoid dendritic cellsR01AI081848 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BHARDWAJ, NINA · 2010 to 2021
$4.5M
Induction of Immunity by Non-Replicating HIV-1R37AI044628 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BHARDWAJ, NINA · 2004 to 2014
$4.2M
HIV Dysregulation of Human Plasmacytoid Dendritic CellsK08AI093153 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI O'BRIEN, MEAGAN P · 2011 to 2015
$659k
Use of a Novel Antigen Loading Platform for Dendritic Cell-Based HIV VaccinesK08AI084578 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI MILLER, ELIZABETH ANNE · 2009 to 2013
$658k
NIAID NIH HHS K08 AI084578NIAID NIH HHS K08 AI093153NIAID NIH HHS K08 AI84578NIAID NIH HHS P01AI05712NIAID NIH HHS P01 AI057127NIAID NIH HHS R01 AI081848NIAID NIH HHS R37 AI044628NIAID NIH HHS U01 AI067854PHS HHS U01 A1067854
6 · The paper itself

Abstract

objectiveMyeloid dendritic cell (mDC) dysfunction during HIV infection may hinder the formation of both innate and adaptive immune responses and contribute to pathogenesis. Our objective was to determine whether circulating factors during chronic HIV infection impair mDC function with respect to secretion of IL-12, a pro-Th1 cytokine, and T-cell stimulatory capacity. Particular focus was placed on the effect of combination antiretroviral therapy (cART) and the role of HIV itself on mDC function.

methodsMonocyte-derived DC (moDC) from uninfected donors were exposed to plasma from HIV-infected individuals before Toll-like receptor (TLR) stimulation. Cytokine secretion was measured via cytokine bead arrays, and T-cell proliferation and IFNγ secretion was evaluated after coculture with naive CD4 T cells. Expression of genes central to TLR-mediated signal transduction was analyzed via quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) arrays and western blot.

resultsExposure of monocyte-derived DC to plasma from untreated HIV-infected donors suppressed secretion of IL-12, and impaired Th1-skewing of CD4 T cells. The suppressive effect was less by plasma donors receiving cART. Removal of virus from plasma did not relieve suppression nor was IL-12 secretion decreased on addition of HIV to control plasma. On a transcriptional level, decreased expression of IKKβ, a key regulator in the TLR/NF-kappaB signaling pathway, corresponded to suppressed cytokine secretion.

conclusionsPlasma factors during chronic HIV infection impair mDC function in a manner that likely impacts the formation of immune responses to HIV, opportunistic pathogens, and vaccines. Despite partial alleviation by cART, this suppression was not directly mediated by HIV.

Indexed as

HIV-1AdultCD4-Positive T-LymphocytesCoculture TechniquesCross-Sectional StudiesDendritic CellsFemaleGene ExpressionHIV InfectionsHumansI-kappa B KinaseImmune ToleranceInterleukin-12MaleMiddle AgedSignal TransductionI-kappa B KinaseInterleukin-12

Identifiers

PMID22902724
PMCPMC3508089
OpenAlexW2048656672

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.