Increased production of tumour necrosis factor alpha in chronic hepatitis B virus infection

Sheron, Nick; Lau, Johnson Y.N.; Daniels, Helena M.; Goka, J.; Eddleston, A. L. W. F.; Alexander, Graeme; Williams, Roger

doi:10.1016/0168-8278(91)90945-8

Cited by 114 publications

(56 citation statements)

References 16 publications

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“…Elevated serum and hepatic levels of TNF␣ (41,42) and TNF␣ receptor p75 (43,44) can be found in patients with acute or chronic hepatitis B. Studies of HBV infection in animal models show that TNF␣ produced by HBV-specific cytotoxic T lymphocytes (CTLs) down-regulates HBV replication in hepatocytes by noncytopathic mechanisms (45).…”

Section: Discussionmentioning

confidence: 99%

Safety of tumor necrosis factor α blockers in hepatitis B virus occult carriers (hepatitis B surface antigen negative/anti–hepatitis B core antigen positive) with rheumatic diseases

Caporali

Bobbio-Pallavicini

Atzeni

et al. 2010

Arthritis Care & Research

117

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Section: Discussionmentioning

confidence: 99%

Safety of tumor necrosis factor α blockers in hepatitis B virus occult carriers (hepatitis B surface antigen negative/anti–hepatitis B core antigen positive) with rheumatic diseases

Caporali

Bobbio-Pallavicini

Atzeni

et al. 2010

Arthritis Care & Research

117

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“…11,[16][17][18][19]32 It has been recently shown FIG 7. Levels of TNF-a mRNA (as a ratio to b-actin) in PBMC that production of TNF-a in the liver takes place not and in the liver in patients with chronic hepatitis C at the end of only in nonparenchymal cells but also in hepatocytes.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor ? gene expression and the response to interferon in chronic hepatitis C

et al. 1996

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Tumor necrosis factor a (TNF-a) is a cytokine with infectious agents and has been shown to exert direct pleiotropic properties that is induced in a variety of antiviral effects. [3][4][5] Although low levels of TNF-a can pathological situations including viral infections. In this contribute to cell protection, excessive amounts may work, we analyzed the expression of TNF-a gene in pa-cause cell damage. 2,6 tients with chronic hepatitis C. Serum TNF-a levels wereThe biosynthesis of TNF-a is tightly regulated by found to be elevated in all chronic hepatitis C patients transcriptional and post-transcriptional mechanisms. 1 including those cases presenting sustained biochemical A variety of viruses have been shown to induce the remission of the disease after interferon therapy. Unexpression of TNF-a in vitro. [6][7][8][9] The accumulation of treated patients with chronic hepatitis C showed in-TNF-a messenger RNA (mRNA) that occur in virus- ever, only about 50% of the treated patients respond to IFN-a therapy with normalization of serum transTumor necrosis factor a (TNF-a) is a cytokine, proaminases, and half of these patients relapse after interduced primarily by activated monocytes and lymphoruption of the treatment. 23 cytes, that possesses pleiotropic properties. 1,2 It particiLittle is known about the mechanisms determining pates in the induction of the immune response to the severity of the liver damage and the response to IFN-a in HCV infection. In this paper, we have studied the presence of HCV RNA in the liver or in PBMC is

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“…39,40 In addition, we have previously demonstrated that the local production of TNF-␣ in HBVinfected liver occurred not only in nonparenchymal cells, but also in hepatocytes. However, the precise mechanism responsible for the enhanced intrahepatic expression of TNF-␣ was not defined.…”

Section: Discussionmentioning

confidence: 99%

The hepatitis B virus X protein up-regulates tumor necrosis factor α gene expression in hepatocytes

et al. 1998

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Increased production of tumour necrosis factor alpha in chronic hepatitis B virus infection

Cited by 114 publications

References 16 publications

Safety of tumor necrosis factor α blockers in hepatitis B virus occult carriers (hepatitis B surface antigen negative/anti–hepatitis B core antigen positive) with rheumatic diseases

Safety of tumor necrosis factor α blockers in hepatitis B virus occult carriers (hepatitis B surface antigen negative/anti–hepatitis B core antigen positive) with rheumatic diseases

Tumor necrosis factor ? gene expression and the response to interferon in chronic hepatitis C

The hepatitis B virus X protein up-regulates tumor necrosis factor α gene expression in hepatocytes

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