Viral and host factors induce macrophage activation and loss of toll-like receptor tolerance in chronic HCV infection.

Citation data:

Gastroenterology, ISSN: 1528-0012, Vol: 133, Issue: 5, Page: 1627-36

Publication Year:
2007
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Citations 146
Citation Indexes 146
Repository URL:
https://escholarship.umassmed.edu/gastroenterology_pp/57; https://works.bepress.com/gyongyi_szabo/43; https://ohsu.pure.elsevier.com/en/publications/4c58019c-28c9-4f34-bab2-7a10c308d04d
PMID:
17916356
DOI:
10.1053/j.gastro.2007.08.003
PMCID:
PMC2593079
Author(s):
Dolganiuc, Angela; Norkina, Oxana; Kodys, Karen; Catalano, Donna; Bakis, Gennadiy; Marshall, Christopher; Mandrekar, Pranoti; Szabo, Gyongyi
Publisher(s):
Elsevier BV
Tags:
Medicine; Gastroenterology; Adult; Case-Control Studies; Endotoxins; Female; Hepacivirus; Hepatitis C, Chronic; Humans; Inflammation; Interferon-gamma; Kupffer Cells; Ligands; Lipopolysaccharides; Macrophage Activation; Macrophages; Male; Middle Aged; Monocytes; NF-kappa B; Toll-Like Receptor 2; Toll-Like Receptor 4; Toll-Like Receptors; Tumor Necrosis Factor-alpha; Viral Core Proteins; Hepatology
article description
Persistent inflammation contributes to progression of liver damage in chronic HCV (cHCV) infection. Repeated exposure to toll-like receptor (TLR) ligands results in tolerance, a protective mechanism aimed at limiting inflammation.