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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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  • Above-average Attention Score compared to outputs of the same age and source (60th percentile)

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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.

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

Mendeley readers

The data shown below were compiled from readership statistics for 70 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 70 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 12 17%
Researcher 6 9%
Student > Bachelor 6 9%
Student > Doctoral Student 5 7%
Student > Master 5 7%
Other 10 14%
Unknown 26 37%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 13 19%
Immunology and Microbiology 9 13%
Agricultural and Biological Sciences 6 9%
Medicine and Dentistry 6 9%
Pharmacology, Toxicology and Pharmaceutical Science 3 4%
Other 6 9%
Unknown 27 39%
Attention Score in Context

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
#15,523,434
of 25,382,440 outputs
Outputs from Journal of Biomedical Science
#650
of 1,101 outputs
Outputs of similar age
#178,255
of 329,774 outputs
Outputs of similar age from Journal of Biomedical Science
#6
of 15 outputs
Altmetric has tracked 25,382,440 research outputs across all sources so far. This one is in the 37th percentile – i.e., 37% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,101 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 11.1. 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 329,774 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 44th percentile – i.e., 44% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 15 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 60% of its contemporaries.