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Hepatocyte-mediated cytotoxicity and host defense mechanisms in the alcohol-injured liver

Overview of attention for article published in Hepatology International, December 2013
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  • Good Attention Score compared to outputs of the same age and source (71st percentile)

Mentioned by

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1 tweeter

Citations

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5 Dimensions

Readers on

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8 Mendeley
Title
Hepatocyte-mediated cytotoxicity and host defense mechanisms in the alcohol-injured liver
Published in
Hepatology International, December 2013
DOI 10.1007/s12072-013-9511-7
Pubmed ID
Authors

Benita L. McVicker, Geoffrey M. Thiele, Dean J. Tuma, Carol A. Casey

Abstract

The consumption of alcohol is associated with many health issues including alcoholic liver disease (ALD). The natural history of ALD involves the development of steatosis, inflammation (steatohepatitis), fibrosis and cirrhosis. During the stage of steatohepatitis, the combination of inflammation and cellular damage can progress to a severe condition termed alcoholic hepatitis (AH). Unfortunately, the pathogenesis of AH remains uncharacterized. Some modulations have been identified in host defense and liver immunity mechanisms during AH that highlight the role of intrahepatic lymphocyte accumulation and associated inflammatory cytokine responses. Also, it is hypothesized that alcohol-induced injury to liver cells may significantly contribute to the aberrant lymphocytic distribution that is seen in AH. In particular, the regulation of lymphocytes by hepatocytes may be disrupted in the alcoholic liver resulting in altered immunologic homeostasis and perpetuation of disease. In recent studies, it was demonstrated that the direct killing of activated T lymphocytes by hepatocytes is facilitated by the asialoglycoprotein receptor (ASGPR). The ASGPR is a well-characterized glycoprotein receptor that is exclusively expressed by hepatocytes. This hepatic receptor is known for its role in the clearance of desialylated glycoproteins or cells, yet neither its physiological function nor its role in disease states has been determined. Interestingly, alcohol markedly impairs ASGPR function; however, the effect alcohol has on ASGPR-mediated cytotoxicity of lymphocytes remains to be elucidated. This review discusses the contribution of hepatocytes in immunological regulation and, importantly, how pathological effects of ethanol disrupt hepatocellular-mediated defense mechanisms.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter 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 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 %
Researcher 3 38%
Student > Postgraduate 1 13%
Professor 1 13%
Student > Ph. D. Student 1 13%
Student > Doctoral Student 1 13%
Other 1 13%
Readers by discipline Count As %
Medicine and Dentistry 3 38%
Agricultural and Biological Sciences 1 13%
Biochemistry, Genetics and Molecular Biology 1 13%
Immunology and Microbiology 1 13%
Chemistry 1 13%
Other 1 13%

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 24 July 2015.
All research outputs
#8,169,888
of 13,028,155 outputs
Outputs from Hepatology International
#102
of 211 outputs
Outputs of similar age
#123,196
of 233,537 outputs
Outputs of similar age from Hepatology International
#3
of 14 outputs
Altmetric has tracked 13,028,155 research outputs across all sources so far. This one is in the 23rd percentile – i.e., 23% of other outputs scored the same or lower than it.
So far Altmetric has tracked 211 research outputs from this source. They receive a mean Attention Score of 2.6. This one is in the 45th percentile – i.e., 45% 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 233,537 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 37th percentile – i.e., 37% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 14 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 71% of its contemporaries.