Evidence map›Paper›PMID 26268402›Full record

ArticleBMC immunology2015

Impairment of dendritic cell function and induction of CD4(+)CD25(+)Foxp3(+) T cells by excretory-secretory products: a potential mechanism of immune evasion adopted by Echinococcus granulosus.

Ying Wang, Hejun Zhou, Yujuan Shen, Yanjuan Wang, Weiping Wu, Haipeng Liu, Zhongying Yuan, Yuxin Xu, Yuan Hu, Jianping Cao

Open access · goldAbstract read
In one paragraph

Article in BMC immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 54 citations in OpenAlex.

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  15. Frontiers in cellular and infection microbiology · 2021
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  16. Metabolomics Analysis of Splenic CD19Frontiers in veterinary science · 2021
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  17. Review
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  20. Frontiers in immunology · 2019
    Article
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

10 authors at 1 institution in 1 country.

Ying WangNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention; Laboratory of Parasite and Vector Biology, MOH, China, WHO Collaborating Center for Malaria, Schistosomiasis and Filariasis, Shanghai, 200025, PR China. wangying1162@163.com.
Hejun ZhouNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention; Laboratory of Parasite and Vector Biology, MOH, China, WHO Collaborating Center for Malaria, Schistosomiasis and Filariasis, Shanghai, 200025, PR China. zhouhejun2@126.com.
Yujuan ShenNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention; Laboratory of Parasite and Vector Biology, MOH, China, WHO Collaborating Center for Malaria, Schistosomiasis and Filariasis, Shanghai, 200025, PR China. amyshyj12@163.com.
Yanjuan WangNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention; Laboratory of Parasite and Vector Biology, MOH, China, WHO Collaborating Center for Malaria, Schistosomiasis and Filariasis, Shanghai, 200025, PR China. wangyanjuan1036@126.com.
Weiping WuNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention; Laboratory of Parasite and Vector Biology, MOH, China, WHO Collaborating Center for Malaria, Schistosomiasis and Filariasis, Shanghai, 200025, PR China. wuweiping@hotmail.com.
Haipeng LiuNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention; Laboratory of Parasite and Vector Biology, MOH, China, WHO Collaborating Center for Malaria, Schistosomiasis and Filariasis, Shanghai, 200025, PR China. haipeng26@gmail.com.
Zhongying YuanNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention; Laboratory of Parasite and Vector Biology, MOH, China, WHO Collaborating Center for Malaria, Schistosomiasis and Filariasis, Shanghai, 200025, PR China. yuanzhy0606@aliyun.com.
Yuxin XuNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention; Laboratory of Parasite and Vector Biology, MOH, China, WHO Collaborating Center for Malaria, Schistosomiasis and Filariasis, Shanghai, 200025, PR China. ipdxuyx@163.com.
Yuan HuNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention; Laboratory of Parasite and Vector Biology, MOH, China, WHO Collaborating Center for Malaria, Schistosomiasis and Filariasis, Shanghai, 200025, PR China. huyuan7576@sina.com.
Jianping CaoNational Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention; Laboratory of Parasite and Vector Biology, MOH, China, WHO Collaborating Center for Malaria, Schistosomiasis and Filariasis, Shanghai, 200025, PR China. caojp@yahoo.com.
National Institute for Parasitic Diseases · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCystic echinococcosis, caused by infection with Echinococcus granulosus, is one of the most widespread zoonotic helminth diseases. Modulation of host responses is an important strategy used by helminth parasites to promote infection. To better understand the mechanisms adopted by E. granulosus to escape host immune responses, we investigated the effects of excretory-secretory products (ES) and adult worm antigen (AWA) derived from adult E. granulosus on murine bone marrow-derived dendritic cells (BMDC).

resultsCompared with lipopolysaccharide (LPS), AWA, but not ES, induced BMDC maturation or stimulated BMDC cytokine production and co-stimulatory molecule expression (CD40, CD80 and MHC class II). Furthermore, ES-treated BMDCs pulsed with ovalbumin exhibited reduced co-stimulatory molecule expression in comparison with untreated BMDC, even in the presence of the strong Th1 inducer, CpG. Moreover, we detected the effects of ES-treated DC on T cell activation by an in vitro T cell priming assay. We observed that ES-treated BMDC co-cultured with DO11.10 transgenic CD4(+) T cells induced the generation of CD4(+)CD25(+)Foxp3(+) T cells. In addition, in contrast to AWA-treated BMDCs, which had markedly induced IFN-γ secretion and reduced of IL-4 levels in co-cultured T cells, ES-treated BMDCs did not modify their capacity to stimulate IFN-γ or IL-4 production by T cells.

conclusionsWe conclude that ES of adult E. granulosus inhibited DC function, impaired the development of Th1 cells induced by CpG, and induced CD4(+)CD25(+)Foxp3(+) regulatory T cells in an IL-10-independent manner.

Indexed as

AnimalsAntigens, CDAntigens, HelminthBone Marrow CellsCell DifferentiationCoculture TechniquesCytokinesDendritic CellsEchinococcus granulosusForkhead Transcription FactorsImmune EvasionLigandsMice, Inbred BALB CMice, TransgenicOvalbuminPhenotypeAntigens, CDAntigens, HelminthCytokinesForkhead Transcription FactorsFoxp3 protein, mouseLigandsOvalbuminToll-Like Receptors

Identifiers

PMID26268402
PMCPMC4535532
OpenAlexW1918013898

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.