Sentence examples for mediate liver damage from inspiring English sources

In liver, cytokines and reactive oxygen and nitrogen species produced by inflammatory cells have been shown to mediate liver damage and induce the liver's regenerative response [ 22- 26].

NK cells have been shown to mediate liver damage in a number of diseases, including primary biliary cirrhosis (Chuang et al. 2008), infection with pseudomona aeruginosa or staphylococcal-induced hepatotoxicity (Notas et al. 2009).

Although these data strongly support the use of T cells for gene therapy in CHB patients, restoring HBV-specific T-cell immunity may potentially mediate liver damage through the triggering of an intrahepatic inflammatory response.

Perpetuation of this inflammatory cascade and immune cell mediated liver damage is thought to induce subsequent fibrosis.

Moreover, the induction of TLR4 was implicated as the molecular mechanism mediating liver damage and tumor formation in alcohol abused patients [ 57].

ConA-induced liver injury in mice is a well-established model for investigating the pathophysiological process of autoimmune or viral fulminant hepatitis, in which acute immune responses have a pivotal role in mediating liver damage.

Since hepatic T and NK cells from infected WSX-1-/ mice produce more IFN-γ and tumor necrosis factor (TNF -α TNF -αild-than cohorts and in vivo neutralization of IFN-γ can ameliorate pathology in receptor deficient animals, it is likely that dysregulated Th1 responses mediate the liver damage (Fig. 3) [ 53].

This interaction leads to suppression of T-cell responses and knockout mice lacking LSECtin show increased sensitivity to liver damage mediated by T cells following acute injury, suggesting that LSECtin plays a role in protection of the liver from immune attack (Tang et al. 2009).

As HBV is a noncytopathic virus, HBV-specific T-cell recognition of infected hepatocytes is believed to mediate both virus control and liver damage [ 7].

Given the critical role of JNK and Bim in various forms of hepatocyte apoptosis, and the similarity between APAP-induced liver damage and hepatitis mediated by the apoptosis pathway, we explored in this study the role of death receptor-induced JNK and associated Bim activation in APAP-induced liver damage.

Although liver damage is initiated and mediated by the CTLs, antigen-nonspecific inflammatory cells can worsen CTL-induced immunopathology, and platelets activated at the site of infection may facilitate the accumulation of CTLs in the liver.