Evidence map›Paper›PMID 22516958›Full record

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

Engineering DNA nanoparticles as immunomodulatory reagents that activate regulatory T cells.

Lei Huang, Henrique P Lemos, Lingqian Li, MingHui Li, Phillip R Chandler, Babak Baban, Tracy L McGaha, Buvana Ravishankar, Jeffrey R Lee, David H Munn and 1 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 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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.

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

52 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
  2. Immunoregulatory properties of cell free DNA.Cellular and molecular life sciences : CMLS · 2025
    Article
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  6. The balance between gasdermin D and STING signaling shapes the severity of schistosome immunopathology.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

11 authors at 1 institution in 1 country.

Lei HuangImmunotherapy Center, Georgia Health Sciences University, Augusta, GA 30912, USA.
Henrique P Lemos
Lingqian Li
MingHui Li
Phillip R Chandler
Babak Baban
Tracy L McGaha
Buvana Ravishankar
Jeffrey R Lee
David H Munn
Andrew L Mellor
Augusta University Health · US

Funding

Engineering DNA nanoparticles to create immune toleranceR01AI103347 · NIAID · AUGUSTA UNIVERSITY · PI MELLOR, ANDREW LEE · 2013 to 2016
$1.5M
IDO dependent T cell suppressionR01AI063402 · NIAID · MEDICAL COLLEGE OF GEORGIA (MCG) · PI MELLOR, ANDREW LEE · 2005 to 2009
$1.4M
T cell regulation by IDO-competent plasmacytoid dendritic cellsR01AI075165 · NIAID · AUGUSTA UNIVERSITY · PI MELLOR, ANDREW LEE · 2009 to 2010
$735k
NIAID NIH HHS AI075165NIAID NIH HHS R01 AI063402NIAID NIH HHS R01 AI075165NIAID NIH HHS R01 AI103347
6 · The paper itself

Abstract

Nanoparticles containing DNA complexed with the cationic polymer polyethylenimine are efficient vehicles to transduce DNA into cells and organisms. DNA/polyethylenimine nanoparticles (DNPs) also elicit rapid and systemic release of proinflammatory cytokines that promote antitumor immunity. In this study, we report that DNPs possess previously unrecognized immunomodulatory attributes due to rapid upregulation of IDO enzyme activity in lymphoid tissues of mice. IDO induction in response to DNP treatment caused dendritic cells and regulatory T cells (Tregs) to acquire potent regulatory phenotypes. As expected, DNP treatment stimulated rapid increase in serum levels of IFN type I (IFN-αβ) and II (IFN-γ), which are both potent IDO inducers. IDO-mediated Treg activation was dependent on IFN type I receptor signaling, whereas IFN-γ receptor signaling was not essential for this response. Moreover, systemic IFN-γ release was caused by TLR9-dependent activation of NK cells, whereas TLR9 signaling was not required for IFN-αβ release. Accordingly, DNPs lacking immunostimulatory TLR9 ligands in DNA stimulated IFN-αβ production, induced IDO, and promoted regulatory outcomes, but did not stimulate potentially toxic, systemic release of IFN-γ. DNP treatment to induce IDO and activate Tregs blocked Ag-specific T cell responses elicited in vivo following immunization and suppressed joint pathology in a model of immune-mediated arthritis. Thus, DNPs lacking TLR9 ligands may be safe and effective reagents to protect healthy tissues from immune-mediated destruction in clinical hyperimmune syndromes.

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidCells, CulturedCytokinesDendritic CellsDNA, BacterialGenetic EngineeringImmunologic FactorsImmunophenotypingIndoleamine-Pyrrole 2,3,-DioxygenaseLymphocyte ActivationMiceMice, Inbred C57BLMice, TransgenicNanoparticlesCytokinesDNA, BacterialImmunologic FactorsIndoleamine-Pyrrole 2,3,-DioxygenasePolydeoxyribonucleotidesPolyethyleneimine

Identifiers

PMID22516958
PMCPMC3349160
OpenAlexW2166712548

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.