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Liver FOXP3 and PD1/PDL1 Expression is Down-Regulated in Chronic HBV Hepatitis on Maintained Remission Related to the Degree of Inflammation

Overview of attention for article published in Frontiers in immunology, January 2013
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Title
Liver FOXP3 and PD1/PDL1 Expression is Down-Regulated in Chronic HBV Hepatitis on Maintained Remission Related to the Degree of Inflammation
Published in
Frontiers in immunology, January 2013
DOI 10.3389/fimmu.2013.00207
Pubmed ID
Authors

Georgios Germanidis, Nikoletta Argentou, Prodromos Hytiroglou, Themistoklis Vassiliadis, Kalliopi Patsiaoura, Anastasios E. Germenis, Matthaios Speletas

Abstract

Background and Aim: T cell expression of PD1 and inhibition of T effector cells by Foxp3(+)-T regulatory cells are among the most powerful mechanisms for achieving a balanced immune response. Our aim was to investigate, how liver FOXP3 and PD1/PDL1 expression is regulated in chronic HBV hepatitis (CHB) on maintained long-term remission in comparison with active disease, and whether they are correlated to the expression of pro- and anti-inflammatory cytokines and apoptosis mediators, along with the degree of histological inflammation and markers of T cell effector restoration. Methods: Fifty-three HBeAg-negative CHB patients with both active (30) and completely remitted disease on long-term antiviral treatment (23) and four controls (submitted to liver biopsy due to a mild increase of aminotransferases but without liver necroinflammatory and architecture changes) were enrolled in the study. Liver mRNA levels of immunoregulatory genes (FOXP3, IL10, TGFB1, and those of PD1/PDL1/PDL2 pathway), major apoptosis mediators (FAS, FASL, TNFA, TRAIL), cytokines of effector T cell restoration (IL2, IFNG), and those of IL1B, CD4, and CD8, were evaluated by quantitative real-time reverse-transcriptase PCR and were correlated with each other, along with the intensity of liver inflammation and fibrosis staging. The expression and localization of FOXP3, PD1, PDL1, CD4, and CD8 were also assessed by immunohistochemistry. Results: The expression of FOXP3, IL10, TGFB1, PD1, PDL1, FASL, and CD8 was significantly down-regulated in the remission state. In contrast, liver expression of IL2 and IFNG, along with CD4, IL1B, TNFA, and FAS did not change significantly. Moreover, FOXP3, PD1, PDL1, and CD8 transcripts were positively correlated to the intensity of liver inflammation. Conclusion: Our data indicate that in the CHB disease model, the immunosuppressive liver environment is down-regulated in the maintained on-treatment long-term remission state and correlates with the intensity of liver inflammation, but not liver T cell restoration.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 44 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 44 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 8 18%
Student > Master 8 18%
Researcher 7 16%
Professor 4 9%
Other 2 5%
Other 5 11%
Unknown 10 23%
Readers by discipline Count As %
Medicine and Dentistry 12 27%
Agricultural and Biological Sciences 11 25%
Immunology and Microbiology 5 11%
Environmental Science 1 2%
Biochemistry, Genetics and Molecular Biology 1 2%
Other 2 5%
Unknown 12 27%
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 31 July 2013.
All research outputs
#20,345,004
of 25,870,940 outputs
Outputs from Frontiers in immunology
#23,096
of 32,522 outputs
Outputs of similar age
#224,022
of 291,559 outputs
Outputs of similar age from Frontiers in immunology
#240
of 503 outputs
Altmetric has tracked 25,870,940 research outputs across all sources so far. This one is in the 18th percentile – i.e., 18% of other outputs scored the same or lower than it.
So far Altmetric has tracked 32,522 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.5. This one is in the 22nd percentile – i.e., 22% 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 291,559 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 20th percentile – i.e., 20% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 503 others from the same source and published within six weeks on either side of this one. This one is in the 36th percentile – i.e., 36% of its contemporaries scored the same or lower than it.