Evidence map›Paper›PMID 38453639›Full record

ArticleJournal of Zhejiang University. Science. B2024

Newcastle disease virus suppresses antigen presentation via inhibiting IL-12 expression in dendritic cells.

Fulong Nan, Wenlong Nan, Xin Yan, Hui Wang, Shasha Jiang, Shuyun Zhang, Zhongjie Yu, Xianjuan Zhang, Fengjun Liu, Jun Li and 11 more

Open access · greenAbstract read
In one paragraph

Article in Journal of Zhejiang University. Science. B, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 95% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. Immune cell disorder in viral pneumonia.Journal of translational medicine · 2026
    Review
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

21 authors at 8 institutions in 1 country.

Fulong NanDepartment of Special Medicine, Department of Pathogenic Biology, School of Basic Medicine, Qingdao University, Qingdao 266071, China.
Wenlong NanChina Animal Health and Epidemiology Center, Qingdao 266032, China.
Xin YanChina Animal Health and Epidemiology Center, Qingdao 266032, China.
Hui WangDepartment of Special Medicine, Department of Pathogenic Biology, School of Basic Medicine, Qingdao University, Qingdao 266071, China.
Shasha JiangDepartment of Special Medicine, Department of Pathogenic Biology, School of Basic Medicine, Qingdao University, Qingdao 266071, China.
Shuyun ZhangDepartment of Special Medicine, Department of Pathogenic Biology, School of Basic Medicine, Qingdao University, Qingdao 266071, China.
Zhongjie YuSino-Cell Biomed Co., Ltd., Qingdao 266000, China.
Xianjuan ZhangDepartment of Special Medicine, Department of Pathogenic Biology, School of Basic Medicine, Qingdao University, Qingdao 266071, China.
Fengjun LiuDepartment of Special Medicine, Department of Pathogenic Biology, School of Basic Medicine, Qingdao University, Qingdao 266071, China.
Jun LiDepartment of Special Medicine, Department of Pathogenic Biology, School of Basic Medicine, Qingdao University, Qingdao 266071, China.
Xiaoqiong ZhouDepartment of Special Medicine, Department of Pathogenic Biology, School of Basic Medicine, Qingdao University, Qingdao 266071, China.
Delei NiuDepartment of Special Medicine, Department of Pathogenic Biology, School of Basic Medicine, Qingdao University, Qingdao 266071, China.
Yiquan LiAcademician Workstation of Jilin Province, Changchun University of Chinese Medicine, Changchun 130117, China.
Wei WangInstitute of Virology, Wenzhou University, Wenzhou 325035, China.
Ning ShiCollege of Veterinary Medicine, Jilin University, Changchun 130012, China.
Ningyi JinChangchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun 130122, China.
Changzhan XieChangchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun 130122, China.
Xiaoni CuiSino-Cell Biomed Co., Ltd., Qingdao 266000, China.
He ZhangChangchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun 130122, China.
Bin WangDepartment of Special Medicine, Department of Pathogenic Biology, School of Basic Medicine, Qingdao University, Qingdao 266071, China. Wangbin532@126.com.
Huijun LuChangchun Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Changchun 130122, China. huijun_lu@126.com.
Qingdao University · CNChinese Academy of Agricultural Sciences · CNChina Animal Health and Epidemiology Center · CNSino Biological (China) · CNChangchun Institute of Optics, Fine Mechanics and Physics · CNChangchun University of Chinese Medicine · CNJilin University · CNWenzhou University · CN

Funding

the Qingdao Municipal Science and Technology Foundation 20-2-3-4-nshthe Qingdao Postdoctoral Application Research Project RZ2200001472the Shandong Provincial Innovative Ability Improvement Project of Scientific and Technological Small and Medium-Size Enterprise 2022TSGC1142the Shandong Provincial Science and Technology Foundation 2019JZZY011009
6 · The paper itself

Abstract

As a potential vectored vaccine, Newcastle disease virus (NDV) has been subject to various studies for vaccine development, while relatively little research has outlined the immunomodulatory effect of the virus in antigen presentation. To elucidate the key inhibitory factor in regulating the interaction of infected dendritic cells (DCs) and T cells, DCs were pretreated with the NDV vaccine strain LaSota as an inhibitor and stimulated with lipopolysaccharide (LPS) for further detection by enzyme-linked immunosorbent assay (ELISA), flow cytometry, immunoblotting, and quantitative real-time polymerase chain reaction (qRT-PCR). The results revealed that NDV infection resulted in the inhibition of interleukin (IL)-12p40 in DCs through a p38 mitogen-activated protein kinase (MAPK)‍-dependent manner, thus inhibiting the synthesis of IL-12p70, leading to the reduction in T cell proliferation and the secretion of interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and IL-6 induced by DCs. Consequently, downregulated cytokines accelerated the infection and viral transmission from DCs to T cells. Furthermore, several other strains of NDV also exhibited inhibitory activity. The current study reveals that NDV can modulate the intensity of the innate‍‒‍adaptive immune cell crosstalk critically toward viral invasion improvement, highlighting a novel mechanism of virus-induced immunosuppression and providing new perspectives on the improvement of NDV-vectored vaccine.

Indexed as

Newcastle disease virusVaccinesAnimalsAntigen PresentationDendritic CellsInterleukin-12Interleukin-12VaccinesDendritic cellsImmunosuppressionInterleukin-12 (IL-12)Newcastle disease virusT cells

Identifiers

PMID38453639
PMCPMC10918410
OpenAlexW4392866752

What OpenQuestion holds

Textmetadata
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.