Results 61 to 70 of about 459,041 (305)

CHB‐Induced Immune Zonation Chaos Elicited LXRα‐mediated Lipid Metabolism Disorders in Kupffer Cells to Induce Cancer Stem Cell Formation

open access: yesAdvanced Science, EarlyView.
By profiling the spatiotemporal hepatic landscape of CHB mouse models, the originally peri‐portal localized KCs migrated to the peri‐central in a CXCL9‐CXCR3‐dependent manner, facilitating their interaction with HBV+ hepatocytes. The interaction promoted LMD in KCs through ASGR1‐induced LXRα degradation, which, in turn, induced CSC formation via Stat3 ...
Jingqi Shi   +18 more
wiley   +1 more source

Chronic Viral Hepatitis: Etiology, Pathogenesis of Liver Damage and Mechanisms of Persistence [PDF]

open access: yes, 2004
Chronic hepatotropic viruses commonly evade the antiviral defence systems of the body and cause a long - lasting persistent infection. The prolonged nature of the infection ensures that every infected person has ample opportunity to transmit the virus to
Setiabudi, I. (Irwan)
core  

p16Ink4a‐Positive Hepatocytes Drive Liver Fibrosis Through Activation of LIFR Family Pathway

open access: yesAdvanced Science, EarlyView.
This study found that, following the long‐term CCl4 treatment, p16high hepatocytes appeared in zone 3, spatially co‐localizing with fibrotic areas. A specific cluster of p16high hepatocytes upregulated CTF1/LIF expression which induced HSC activation and further liver fibrosis, as revealed by single cell transcriptomic analysis.
Koji Nishikawa   +23 more
wiley   +1 more source

Initiation of hepatitis C virus infection is dependent on cholesterol and cooperativity between CD81 and scavenger receptor B type I. [PDF]

open access: yes, 2006
In the past several years, a number of cellular proteins have been identified as candidate entry receptors for hepatitis C virus (HCV) by using surrogate models of HCV infection.
Barth, Heidi   +4 more
core   +2 more sources

Nuclear Factor I‐B Delays Liver Fibrosis by Inhibiting Chemokine Ligand 5 Transcription

open access: yesAdvanced Science, EarlyView.
This study identifies the transcription factor Nuclear Factor I‐B (NFIB) as a key suppressor of liver fibrosis. NFIB expression declines during hepatic stellate cell activation, and its overexpression reduces fibrosis in mice models. The mechanism involves NFIB directly repressing chemokine C─C motif ligand 5 (CCL5), thereby alleviating oxidative ...
Qianqian Chen   +14 more
wiley   +1 more source

Requirement of Activation for Hepatitis B Virus Infection [PDF]

open access: yes, 2007
Although _in vitro_ models of human hepatitis B virus replication are established, so far none could approximate infection efficiency as expected from _in vivo_ observations.
Claudia Maenz, Michael Bruns
core   +1 more source

Pathogenesis of hepatitis B virus infection [PDF]

open access: yesWorld Journal of Gastroenterology, 2007
Infection with hepatitis B virus (HBV) leads to a wide spectrum of clinical presentations ranging from an asymptomatic carrier state to self-limited acute or fulminant hepatitis to chronic hepatitis with progression to cirrhosis and hepatocellular carcinoma. Infection with HBV is one of the most common viral diseases affecting man.
Thomas F, Baumert   +2 more
openaire   +2 more sources

Inhibition of SLC11A1‐Mediated Lysosomal Iron Accumulation in Microglia Promotes Repair Following White Matter Stroke

open access: yesAdvanced Science, EarlyView.
Genetic and pharmacological inhibition of SLC11A1 functioning as an H+/Fe2+ antiporter–mediated lysosomal iron accumulation in microglia promotes lysosomal lumen acidification, increases CTSD expression, enhances lysosomal myelin debris uptake and degradation, and promotes repair following white matter stroke. ABSTRACT White matter stroke (WMS) results
Lingling Qiu   +11 more
wiley   +1 more source

Host–virus interactions in hepatitis B virus infection [PDF]

open access: yesCurrent Opinion in Immunology, 2015
Hepatitis B virus (HBV) is a noncytopathic, hepatotropic, double-stranded DNA virus that causes acute and chronic hepatitis. Although HBV does not induce a measurable innate immune response in the infected liver, the outcome of infection is determined by the kinetics, breadth, vigor, trafficking, and effector functions of HBV-specific adaptive T cell ...
Guidotti, LG   +2 more
openaire   +3 more sources

Cleavage‐Resistant CYLD Protects Against Autoimmune Hepatitis

open access: yesAdvanced Science, EarlyView.
Proteolytic cleavage of the deubiquitinase CYLD emerges as a critical driver of autoimmune hepatitis. TNFα‐induced CYLD loss in macrophages amplifies S100A9‐triggered MAPK activation, leading to excessive chemokine production and hepatic inflammation. Pharmacological inhibition of MEK signaling effectively attenuates experimental disease, highlighting ...
Han Liu   +13 more
wiley   +1 more source

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