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Review
. 2001 Dec;82(6):317-26.
doi: 10.1046/j.1365-2613.2001.00207.x.

The effect of IFNgamma on the hepatocyte: cell cycle and apoptosis

B J Tura  1 , K E Bunyan, D J Harrison
Affiliations
Review

The effect of IFNgamma on the hepatocyte: cell cycle and apoptosis

B J Tura et al. Int J Exp Pathol. 2001 Dec.

Abstract

The inflammatory cytokine interferon gamma (IFNgamma) can cause cell cycle arrest and apoptosis in the hepatocyte. Primarily these processes are protective but in chronic liver disease oncogenic mutations may prosper. IFNgamma signalling is discussed showing how p53 is induced to cause cell cycle arrest. While caspases are are known to be responsible for IFNgamma induced apoptosis, how they are activated is unclear. Potential mechanisms are reviewed.

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Figures

Figure 1
Figure 1
The binding of IFNγ to the cell surface receptor causes dimerization of STAT-1, forming the GAF. Translocation of the GAF to the nucleus allows transcription of IRF-1. IRF-1 is necessary for hepatocyte cell cycle arrest, mediated primarily through the action of the cyclin inhibitor, p21, on cyclin D1 and cyclin E. IRF-1 and p53 may synergistically increase p21 transcription. IRF-2 has an antagonistic function to IRF-1, blocking transcription of IRF-1 dependant genes.
Figure 2
Figure 2
(a) The induction of inflammation. (b) Acute HBV infection. (c) Chronic hepatitis. (d) Key.
See this image and copyright information in PMC

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