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Up-regulation of A20/ABIN1 contributes to inefficient M1 macrophage polarization during Hepatitis C virus infection

Overview of attention for article published in Virology Journal, September 2015
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  • Above-average Attention Score compared to outputs of the same age (57th percentile)
  • Above-average Attention Score compared to outputs of the same age and source (51st percentile)

Mentioned by

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3 tweeters

Citations

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16 Dimensions

Readers on

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28 Mendeley
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Title
Up-regulation of A20/ABIN1 contributes to inefficient M1 macrophage polarization during Hepatitis C virus infection
Published in
Virology Journal, September 2015
DOI 10.1186/s12985-015-0379-0
Pubmed ID
Authors

Chao Fan, Ying Zhang, Yun Zhou, Bingjie Li, Yu He, Yonghong Guo, Zhansheng Jia

Abstract

Anti-hepatitis C virus (HCV) responses are often accompanied by an increase in alanine aminotransferase levels in HCV-infected patients, indicating that inflammatory responses are compromised by the virus. Additionally, inflammation is associated with M1-polarizated macrophages, which secrete cytokines such as tumor necrosis factor-α, interleukin-1, and interleukin-12, and present antigens through phagocytosis. HCV-encoded proteins are presented as specific viral antigens in particular infectious steps that influence the immune response. For instance, HCV antigens impact macrophage PD-1 and Tim-3 expression, and contribute to impaired viral clearance. Furthermore, circulatory HCV antigens from infected patients inhibit dendritic cell differentiation, which raises the possibility that HCV antigens may also interfere with macrophage polarization. In this study, the impact of HCV antigen stimulation on M1-polarized macrophages was investigated. The influence of HCV antigens was evaluated by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay. Specific changes were investigated clinically by flow cytometry and immunofluorescence. Effects of NF-κB during the process were analyzed by western blot. HCV infection dampened M1 macrophage polarization ex vivo and in vitro. After antigen stimulation, NF-κB signaling was suppressed by the up-regulation of A20 and A20-binding inhibitor of NF-κB binding protein, which likely leads to a variation of functional molecules such as tumor necrosis factor-α, CD163, matrix metalloproteinases, transferrin receptor-1, and CD100, reflecting an anti-inflammatory reaction against M1-polarization. HCV antigens stimulation up-regulates A20/A20-binding inhibitor of NF-κB binding protein expression, which consequently contributes to inefficient M1 macrophage polarization.

Twitter Demographics

The data shown below were collected from the profiles of 3 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 28 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Belgium 1 4%
Unknown 27 96%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 7 25%
Researcher 5 18%
Student > Master 4 14%
Student > Bachelor 2 7%
Student > Doctoral Student 2 7%
Other 4 14%
Unknown 4 14%
Readers by discipline Count As %
Medicine and Dentistry 8 29%
Immunology and Microbiology 5 18%
Agricultural and Biological Sciences 5 18%
Biochemistry, Genetics and Molecular Biology 2 7%
Decision Sciences 1 4%
Other 1 4%
Unknown 6 21%

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 12 May 2016.
All research outputs
#3,415,831
of 7,690,302 outputs
Outputs from Virology Journal
#683
of 1,595 outputs
Outputs of similar age
#94,120
of 232,401 outputs
Outputs of similar age from Virology Journal
#27
of 64 outputs
Altmetric has tracked 7,690,302 research outputs across all sources so far. This one has received more attention than most of these and is in the 54th percentile.
So far Altmetric has tracked 1,595 research outputs from this source. They receive a mean Attention Score of 3.4. This one has gotten more attention than average, scoring higher than 52% of its peers.
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 232,401 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 57% of its contemporaries.
We're also able to compare this research output to 64 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 51% of its contemporaries.