↓ Skip to main content

Notch Signaling Contributes to Liver Inflammation by Regulation of Interleukin-22-Producing Cells in Hepatitis B Virus Infection

Overview of attention for article published in Frontiers in Cellular and Infection Microbiology, October 2016
Altmetric Badge

About this Attention Score

  • Average Attention Score compared to outputs of the same age and source

Mentioned by

twitter
2 X users

Citations

dimensions_citation
32 Dimensions

Readers on

mendeley
8 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
Notch Signaling Contributes to Liver Inflammation by Regulation of Interleukin-22-Producing Cells in Hepatitis B Virus Infection
Published in
Frontiers in Cellular and Infection Microbiology, October 2016
DOI 10.3389/fcimb.2016.00132
Pubmed ID
Authors

Xin Wei, Jiu-Ping Wang, Chun-Qiu Hao, Xiao-Fei Yang, Lin-Xu Wang, Chang-Xing Huang, Xue-Fan Bai, Jian-Qi Lian, Ye Zhang

Abstract

The mechanism of hepatitis B virus (HBV) induced liver inflammation is not fully elucidated. Notch signaling augmented interleukin (IL)-22 secretion in CD4(+) T cells, and Notch-IL-22 axis fine-tuned inflammatory response. We previously demonstrated a proinflammatory role of IL-22 in HBV infection. Thus, in this study, we analyzed the role of Notch in development of IL-22-producing cells in HBV infection by inhibition of Notch signaling using γ-secretase inhibitor DAPT in both hydrodynamic induced HBV-infected mouse model and in peripheral blood cells isolated from patients with HBV infection. mRNA expressions of Notch1 and Notch2 were significantly increased in livers and CD4(+) T cells upon HBV infection. Inhibition of Notch signaling in vivo leaded to the reduction in NKp46(+) innate lymphoid cells 22 (ILC22) and lymphoid tissue inducer 4 (LTi4) cells in the liver. This process was accompanied by downregulating the expressions of IL-22 and related proinflammatory cytokines and chemokines in the liver, as well as blocking the recruitment of antigen-non-specific inflammatory cells into the liver and subsequent liver injury, but did not affect HBV antigens production and IL-22 secretion in the serum. Furthermore, IL-22 production in HBV non-specific cultured CD4(+) T cells, but not HBV-specific CD4(+) T cells, was reduced in response to in vitro inhibition of Notch signaling. In conclusion, Notch siganling appears to be an important mediator of the liver inflammation by modulating hepatic ILC22. The potential proinflammatory effect of Notch-mediated ILC22 may be significant for the development of new therapeutic approaches for treatment of hepatitis B.

X Demographics

X Demographics

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.
As of 1 July 2024, you may notice a temporary increase in the numbers of X profiles with Unknown location. Click here to learn more.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 8 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 8 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 2 25%
Student > Bachelor 1 13%
Student > Doctoral Student 1 13%
Researcher 1 13%
Student > Postgraduate 1 13%
Other 0 0%
Unknown 2 25%
Readers by discipline Count As %
Immunology and Microbiology 4 50%
Agricultural and Biological Sciences 1 13%
Biochemistry, Genetics and Molecular Biology 1 13%
Unknown 2 25%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. 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 21 September 2017.
All research outputs
#20,656,820
of 25,374,647 outputs
Outputs from Frontiers in Cellular and Infection Microbiology
#6,021
of 8,068 outputs
Outputs of similar age
#249,054
of 323,025 outputs
Outputs of similar age from Frontiers in Cellular and Infection Microbiology
#38
of 72 outputs
Altmetric has tracked 25,374,647 research outputs across all sources so far. This one is in the 10th percentile – i.e., 10% of other outputs scored the same or lower than it.
So far Altmetric has tracked 8,068 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.8. This one is in the 5th percentile – i.e., 5% 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 323,025 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 12th percentile – i.e., 12% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 72 others from the same source and published within six weeks on either side of this one. This one is in the 38th percentile – i.e., 38% of its contemporaries scored the same or lower than it.