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Decoy receptor 3: an endogenous immunomodulator in cancer growth and inflammatory reactions

Overview of attention for article published in Journal of Biomedical Science, June 2017
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Mentioned by

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2 tweeters

Citations

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23 Dimensions

Readers on

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35 Mendeley
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Title
Decoy receptor 3: an endogenous immunomodulator in cancer growth and inflammatory reactions
Published in
Journal of Biomedical Science, June 2017
DOI 10.1186/s12929-017-0347-7
Pubmed ID
Authors

Shie-Liang Hsieh, Wan-Wan Lin

Abstract

Decoy receptor 3 (DcR3), also known as tumor necrosis factor receptor (TNFR) superfamily member 6b (TNFRSF6B), is a soluble decoy receptor which can neutralize the biological functions of three members of tumor necrosis factor superfamily (TNFSF): Fas ligand (FasL), LIGHT, and TL1A. In addition to 'decoy' function, recombinant DcR3.Fc is able to modulate the activation and differentiation of dendritic cells (DCs) and macrophages via 'non-decoy' action. DcR3-treated DCs skew T cell differentiation into Th2 phenotype, while DcR3-treated macrophages behave M2 phenotype. DcR3 is upregulated in various cancer cells and several inflammatory tissues, and is regarded as a potential biomarker to predict inflammatory disease progression and cancer metastasis. However, whether DcR3 is a pathogenic factor or a suppressor to attenuate inflammatory reactions, has not been discussed comprehensively yet. Because mouse genome does not have DcR3, it is not feasible to investigate its physiological functions by gene-knockout approach. However, DcR3-mediated effects in vitro are determined via overexpressing DcR3 or addition of recombinant DcR3.Fc fusion protein. Moreover, CD68-driven DcR3 transgenic mice are used to investigate DcR3-mediated systemic effects in vivo. Upregulation of DcR3 during inflammatory reactions exerts negative-feedback to suppress inflammation, while tumor cells hijack DcR3 to prevent apoptosis and promote tumor growth and invasion. Thus, 'switch-on' of DcR3 expression may be feasible for the treatment of inflammatory diseases and enhance tissue repairing, while 'switch-off' of DcR3 expression can enhance tumor apoptosis and suppress tumor growth in vivo.

Twitter Demographics

The data shown below were collected from the profiles of 2 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 35 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 35 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 20%
Student > Bachelor 6 17%
Student > Master 4 11%
Student > Postgraduate 3 9%
Researcher 3 9%
Other 8 23%
Unknown 4 11%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 9 26%
Agricultural and Biological Sciences 6 17%
Immunology and Microbiology 4 11%
Medicine and Dentistry 3 9%
Pharmacology, Toxicology and Pharmaceutical Science 3 9%
Other 4 11%
Unknown 6 17%

Attention Score in Context

This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 23 March 2018.
All research outputs
#7,626,530
of 13,791,430 outputs
Outputs from Journal of Biomedical Science
#398
of 676 outputs
Outputs of similar age
#131,262
of 274,377 outputs
Outputs of similar age from Journal of Biomedical Science
#1
of 1 outputs
Altmetric has tracked 13,791,430 research outputs across all sources so far. This one is in the 43rd percentile – i.e., 43% of other outputs scored the same or lower than it.
So far Altmetric has tracked 676 research outputs from this source. They receive a mean Attention Score of 4.9. This one is in the 40th percentile – i.e., 40% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 274,377 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 50% of its contemporaries.
We're also able to compare this research output to 1 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them