scholarly journals Indirect action of tumor necrosis factor-alpha in liver injury during the CD8+ T cell response to an adeno-associated virus vector in mice

Hepatology ◽  
2009 ◽  
Vol 49 (6) ◽  
pp. 2010-2020 ◽  
Author(s):  
Matthew Giannandrea ◽  
Robert H. Pierce ◽  
Ian Nicholas Crispe
Keyword(s):  
Tumor Necrosis Factor ◽  
Liver Injury ◽  
Tumor Necrosis ◽  
Cd8 T Cell ◽  
T Cell Response ◽  
Necrosis Factor Alpha ◽  
Adeno Associated Virus ◽  
Factor Alpha ◽  
Indirect Action ◽  
Necrosis Factor

scholarly journals Neutralization of Tumor Necrosis Factor Alpha Suppresses Antigen-Specific Type 1 Cytokine Responses and Reverses the Inhibition of Mycobacterial Survival in Cocultures of Immune Guinea Pig T Lymphocytes and Infected Macrophages

2005 ◽  
Vol 73 (12) ◽  
pp. 8437-8441 ◽  
Author(s):  
Hyosun Cho ◽  
David N. McMurray
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
T Cell Response ◽  
Interleukin 12 ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT Neutralization of tumor necrosis factor alpha (TNF-α) significantly down-regulated antigen-induced lymphoproliferation and the expression of interleukin-12 p40 and gamma interferon mRNA and enhanced the viability of intracellular attenuated and virulent mycobacteria in cocultures of immune T cells and macrophages obtained from Mycobacterium bovis BCG-vaccinated guinea pigs. This suggests the crucial role of TNF-α in the activation of a type 1 T-cell response against Mycobacterium tuberculosis infection.

scholarly journals Bid-Independent Mitochondrial Activation in Tumor Necrosis Factor Alpha-Induced Apoptosis and Liver Injury

2006 ◽  
Vol 27 (2) ◽  
pp. 541-553 ◽  
Author(s):  
Xiaoyun Chen ◽  
Wen-Xing Ding ◽  
Hong-Min Ni ◽  
Wentao Gao ◽  
Ying-Hong Shi ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Liver Injury ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Apoptosis Pathway ◽  
Tnf Α ◽  
Factor Alpha ◽  
Induced Apoptosis ◽  
Necrosis Factor

ABSTRACT The death receptor apoptosis pathway is intimately connected with the mitochondrial apoptosis pathway. Bid is a BH3-only pro-death Bcl-2 family protein and is the major molecule linking the two pathways. Bid-mediated mitochondrial activation occurs early and is responsible for the prompt progress of tumor necrosis factor alpha (TNF-α)-induced apoptosis. However, in both cultured cells and animal models of TNF-α-induced injury, later-phase Bid-independent mitochondrial activation could be demonstrated. Consequently, bid-deficient mice are still susceptible to endotoxin-induced liver injury and mortality. Notably, embryonic hepatocyte apoptosis and lethality caused by TNF-α in the absence of p65relA cannot be rescued by the simultaneous deletion of bid. Further studies indicate that multiple mechanisms including reactive oxygen species, JNK, and permeability transition are critically involved in Bid-independent mitochondrial activation. Inhibition of these events suppresses TNF-α-induced mitochondrial activation and apoptosis in bid-deficient cells. These findings thus indicate that there are at least two sets of mechanisms of mitochondrial activation upon TNF-α stimulation. While the Bid-mediated mechanism is rapid and potent, the Bid-independent mechanism progresses gradually and involves multiple players. The critical involvement of Bid-independent mitochondrial activation in TNF-α-induced apoptosis demands the intervention of TNF-α-mediated tissue injury via multiple avenues.

scholarly journals Amiodarone Exposure During Modest Inflammation Induces Idiosyncrasy-like Liver Injury in Rats: Role of Tumor Necrosis Factor-alpha

2011 ◽  
Vol 125 (1) ◽  
pp. 126-133 ◽  
Author(s):  
Jingtao Lu ◽  
A. Daniel Jones ◽  
Jack R. Harkema ◽  
Robert A. Roth ◽  
Patricia E. Ganey
Keyword(s):  
Tumor Necrosis Factor ◽  
Liver Injury ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor necrosis factor-alpha induces c-jun during the regenerative response to liver injury

1994 ◽  
Vol 267 (4) ◽  
pp. G552-G561 ◽  
Author(s):  
A. M. Diehl ◽  
M. Yin ◽  
J. Fleckenstein ◽  
S. Q. Yang ◽  
H. Z. Lin ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Liver Injury ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Binding Activity ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

After liver injury, remaining hepatocytes proliferate to regenerate the liver. Although the precise mechanisms that initiate and localize regeneration are unknown, local induction of c-jun is a critical, early step in the response. Treatment of rats with antibodies to tumor necrosis factor-alpha (TNF-alpha), a mediator of liver injury, inhibits regenerative induction of jun nuclear kinase activity and nuclear c-jun expression and alters the DNA binding activity of the c-jun transcription factor, AP-1, in liver. Pretreatment with anti-TNF antibodies does not affect pulmonary or renal c-jun expression or AP-1 binding activity post-partial hepatectomy. In primary hepatocyte cultures, TNF-alpha directly promotes the proliferative actions of mitogens, supporting in vivo evidence that it sensitizes hepatocytes to mitogens. Thus local release of TNF may act in a paracrine fashion to initiate regeneration in the injured liver by promoting induction of critical growth-related genes, such as c-jun.

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