Evidence map›Paper›PMID 23160198›Full record

ArticleThe Journal of clinical investigation2012

HIV-1 infection-induced apoptotic microparticles inhibit human DCs via CD44.

Davor Frleta, Carolyn E Ochoa, Holger B Kramer, Shaukat Ali Khan, Andrea R Stacey, Persephone Borrow, Benedikt M Kessler, Barton F Haynes, Nina Bhardwaj

Registry-linked trialAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02071095 (Simultaneous Disruption of Latency and Immune Enhancement by Poly-ICLC During HIV-1 Infection), which is not on this map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.3field-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.

NCT02071095 phase1 / phase2completednot on this mapstarted 2014, after this paper: background citation

Simultaneous Disruption of Latency and Immune Enhancement by Poly-ICLC During HIV-1 Infection

TypeinterventionalSponsorNina BhardwajRan2014 to 2016Enrolled15ConditionsHIV-1 Infected Adults With Chronic HIV-1 InfectionArmsArm A: Poly-ICLC, Arm B: Normal Saline
3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 46 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Davor FrletaNew York University Langone Medical Center, New York, New York 10016, USA.
Carolyn E Ochoa
Holger B Kramer
Shaukat Ali Khan
Andrea R Stacey
Persephone Borrow
Benedikt M Kessler
Barton F Haynes
Nina Bhardwaj
NYU Langone Health · USUniversity of Oxford · GBDuke University · USJohn Radcliffe Hospital · GB

Funding

Viral Sequencing CoreU19AI067854 · NIAID · DUKE UNIVERSITY · PI CRUMP, JOHN ANDREW · 2006 to 2011
$290.5M
TRAINING PROGRAM IN MOLECULAR ONCOLOGY &IMMUNOLOGYT32CA009161 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CARROLL, WILLIAM L., LEVY, DAVID E · 1985 to 2020
$13.3M
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
Modulating Immunity through Dendritic Cell Phagocytic ReceptorsR01AI071078 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BHARDWAJ, NINA · 2008 to 2011
$1.7M
Immunosuppressive pathways in acute HIV infectionRC1AI087097 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BHARDWAJ, NINA · 2009 to 2010
$959k
NCI NIH HHS T32 CA009161NCI NIH HHS T32CA009161NIAID NIH HHS 5R01AI071078NIAID NIH HHS 5RC1AI087097NIAID NIH HHS 5U19AI067854NIAID NIH HHS R01 AI071078NIAID NIH HHS R01 AI081848NIAID NIH HHS R37 AI044628NIAID NIH HHS RC1 AI087097NIAID NIH HHS U19 AI067854
6 · The paper itself

Abstract

Acute HIV-1 infection results in dysregulated immunity, which contributes to poor control of viral infection. DCs are key regulators of both adaptive and innate immune responses needed for controlling HIV-1, and we surmised that factors elicited during acute HIV-1 infection might impede DC function. We derived immature DCs from healthy donor peripheral blood monocytes and treated them with plasma from uninfected control donors and donors with acute HIV-1 infections. We found that the plasma from patients with HIV specifically inhibited DC function. This suppression was mediated by elevated apoptotic microparticles derived from dying cells during acute HIV-1 infection. Apoptotic microparticles bound to and inhibited DCs through the hyaluronate receptor CD44. These data suggest that targeting this CD44-mediated inhibition by apoptotic microparticles could be a novel strategy to potentiate DC activation of HIV-specific immunity.

Indexed as

ApoptosisCell-Derived MicroparticlesDendritic CellsHIV-1HIV InfectionsHumansHyaluronan ReceptorsImmunity, InnateToll-Like ReceptorsViremiaCD44 protein, humanHyaluronan ReceptorsToll-Like Receptors

Identifiers

PMID23160198
PMCPMC3533550
OpenAlexW2089238809

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.