Evidence map›Paper›PMID 21219617›Full record

ArticleGenetic vaccines and therapy2011

Plasmid-encoded NP73-102 modulates atrial natriuretic peptide receptor signaling and plays a critical role in inducing tolerogenic dendritic cells.

Weidong Zhang, Xueqin Cao, Dongqing Chen, Jia-Wang Wang, Hong Yang, Wenshi Wang, Subhra Mohapatra, Gary Hellermann, Xiaoyuan Kong, Richard F Lockey and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genetic vaccines and therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-weighted citation impact, top 37% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

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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 4 institutions in 1 country.

Weidong Zhang *Department of Internal Medicine, Division of Allergy and Immunology, University of South Florida College of Medicine, Tampa, FL 33612, USA.
Xueqin Cao *Department of Molecular Medicine, University of South Florida College of Medicine, Tampa, FL 33612, USA.
Dongqing ChenDepartment of Internal Medicine, Division of Allergy and Immunology, University of South Florida College of Medicine, Tampa, FL 33612, USA.
Jia-Wang WangJames A. Haley Veterans Hospital Medical Center, Tampa, FL 33612, USA.
Hong YangDepartment of Internal Medicine, Division of Endocrinology, University of South Florida College of Medicine, Tampa, FL 33612, USA.
Wenshi WangDonald A. Adam Comprehensive Melanoma Research Center, Moffitt Cancer Center, 12902 Magnolia Drive, SRB-24324, Tampa, FL 33612, USA.
Subhra MohapatraDepartment of Molecular Medicine, University of South Florida College of Medicine, Tampa, FL 33612, USA.
Gary HellermannDepartment of Internal Medicine, Division of Allergy and Immunology, University of South Florida College of Medicine, Tampa, FL 33612, USA.
Xiaoyuan KongDepartment of Internal Medicine, Division of Allergy and Immunology, University of South Florida College of Medicine, Tampa, FL 33612, USA.
Richard F LockeyDepartment of Internal Medicine, Division of Allergy and Immunology, University of South Florida College of Medicine, Tampa, FL 33612, USA.
Shyam S MohapatraDepartment of Internal Medicine, Division of Allergy and Immunology, University of South Florida College of Medicine, Tampa, FL 33612, USA.
University of South Florida · USFlorida College · USJames A. Haley Veterans' Hospital · USMoffitt Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtrial natriuretic peptide (ANP) is an important endogenous hormone that controls inflammation and immunity by acting on dendritic cells (DCs); however, the mechanism remains unclear.

objectiveWe analyzed the downstream signaling events resulting from the binding of ANP to its receptor, NPRA, and sought to determine what aspects of this signaling modulate DC function.

methodsWe utilized the inhibitory peptide, NP73-102, to block NPRA signaling in human monocyte-derived DCs (hmDCs) and examined the effect on DC maturation and induced immune responses. The potential downstream molecules and interactions among these molecules involved in NPRA signaling were identified by immunoprecipitation and immunoblotting. Changes in T cell phenotype and function were determined by flow cytometry and BrdU proliferation ELISA. To determine if adoptively transferred DCs could alter the in vivo immune response, bone marrow-derived DCs from wild-type C57BL/6 mice were incubated with ovalbumin (OVA) and injected i.v. into C57BL/6 NPRA-/- knockout mice sensitized and challenged with OVA. Lung sections were stained and examined for inflammation and cytokines were measured in bronchoalveolar lavage fluid collected from parallel groups of mice.

resultsInhibition of NPRA signaling in DCs primes them to induce regulatory T cells. Adoptive transfer of wild type DCs into NPRA-/- mice reverses the attenuation of lung inflammation seen in the NPRA-knockout model. NPRA is associated with TLR-2, SOCS3 and STAT3, and inhibiting NPRA alters expression of IL-6, IL-10 and TGF-β, but not IL-12.

conclusionsModulation of NPRA signaling in DCs leads to immune tolerance and TLR2 and SOCS3 are involved in this induction.

Identifiers

PMID21219617
PMCPMC3025824
OpenAlexW2112944444

What OpenQuestion holds

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Registered trials

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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.