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 09 December 2016

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Mechanism underlying the enhanced immune responses in acute-on-chronic Hep B elucidated

The latest issue of the Journal of Gastroenterology evaluates the relevance of the IL-6/signal transducer and activator of transcription 3/mammalian target of rapamycin loop in Hep B-associated acute-on-chronic liver failure.

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Interleukin (IL)-17-producing CD4+ T cells (Th17) have been shown to play crucial roles in the pathogenesis of hepatitis B virus (HBV)-associated acute-on-chronic liver failure.

However, the mechanism underlying the enhanced Th17 responses in these patients remains elusive.

Dr Hee Yeon Kim and colleagues evaluated the relevance of the IL-6/signal transducer and activator of transcription 3 (STAT3)/mammalian target of rapamycin (mTOR)/Th17 loop in HBV-associated  acute-on-chronic liver failure.

The team enrolled 8 patients with HBV-associated acute-on-chronic liver failure, 8 asymptomatic chronic HBV carriers, and 8 healthy controls.

The frequency of peripheral Th17 cells was determined by flow cytometry.

The percentage of peripheral Th17 cells significantly increased in acute-on-chronic liver failure
Journal of Gastroenterology

IL-17 and IL-6 mRNA levels in peripheral blood mononuclear cells were quantified using quantitative real-time reverse polymerase chain reaction.

The team observed the activation of STAT3 upon stimulation with IL-6.

Rapamycin, an mTOR inhibitor, was used for analysis of the suppressive effect on the Th17 response in vitro.

The team found that the percentage of peripheral Th17 cells significantly increased in acute-on-chronic liver failure patients.

CD4+ T cells from acute-on-chronic liver failure patients produced higher levels of IL-17 and IL-6 upon stimulation in vitro.

The researchers noted that the activation of STAT3 in response to IL-6 was elevated in acute-on-chronic liver failure patients.

The IL-6-induced upregulation of IL-17 production by CD4+ T cells could be reversed by an mTOR inhibitor through decreasing STAT3 activation.

Dr Kim's team concludes, "STAT3 activation upon IL-6 stimulation contributed to the enhanced Th17 response in HBV-associated acute-on-chronic liver failure patients and mTOR regulated STAT3 phosphorylation."

"mTOR can be a novel target to suppress Th17-mediated liver injury in HBV-associated acute-on-chronic liver failure patients."

J Gastroenterol 2014: 49(8): 1264-1273
18 August 2014

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