scholarly journals Upregulation of tumor necrosis factor-alpha gene by Epstein-Barr virus and activation of macrophages in Epstein-Barr virus-infected T cells in the pathogenesis of hemophagocytic syndrome.

1997 ◽  
Vol 100 (8) ◽  
pp. 1969-1979 ◽  
Author(s):  
J D Lay ◽  
C J Tsao ◽  
J Y Chen ◽  
M E Kadin ◽  
I J Su
Keyword(s):  
T Cells ◽  
Tumor Necrosis ◽  
Epstein Barr Virus ◽  
Hemophagocytic Syndrome ◽  
Necrosis Factor Alpha ◽  
Barr Virus ◽  
Factor Alpha ◽  
Alpha Gene ◽  
Epstein Barr ◽  
Necrosis Factor

scholarly journals EBNA2 Is Required for Protection of Latently Epstein-Barr Virus-Infected B Cells against Specific Apoptotic Stimuli

2004 ◽  
Vol 78 (22) ◽  
pp. 12694-12697 ◽  
Author(s):  
Jae Myun Lee ◽  
Kyoung-Ho Lee ◽  
Christopher J. Farrell ◽  
Paul D. Ling ◽  
Bettina Kempkes ◽  
...  
Keyword(s):  
B Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Epstein Barr Virus ◽  
Necrosis Factor Alpha ◽  
Barr Virus ◽  
Factor Alpha ◽  
Epstein Barr ◽  
Necrosis Factor ◽  
Transcriptional Transactivator

ABSTRACT In addition to functioning as a transcriptional transactivator, Epstein-Barr virus EBNA2 interacts with Nur77 to protect against Nur77-mediated apoptosis. Estrogen-regulated EBNA2 in EREB2-5 cells was replaced by either EBNA2 or EBNA2 with a deletion of conserved region 4 (EBNA2ΔCR4). Both EBNA2-converted and EBNA2ΔCR4-converted EREB2-5 cells grew in the absence of estrogen and expressed LMP1. Treatment with tumor necrosis factor alpha did not induce apoptosis of EBNA2- or EBNA2ΔCR4-expressing cells, but EBNA2ΔCR4 cells were susceptible to etoposide and 5-fluorouracil, Nur77-mediated inducers of apoptosis. Thus, EBNA2 protects B cells against specific apoptotic agents against which LMP1 is not effective.

Elevated Tumor Necrosis Factor-alpha Expression in Periapical Lesions Infected by Epstein-Barr Virus

2013 ◽  
Vol 39 (4) ◽  
pp. 456-460 ◽  
Author(s):  
Katinka Hernádi ◽  
Eszter Gyöngyösi ◽  
Beáta Mészáros ◽  
Levente Szakács ◽  
Anita Szalmás ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Epstein Barr Virus ◽  
Necrosis Factor Alpha ◽  
Periapical Lesions ◽  
Barr Virus ◽  
Factor Alpha ◽  
Epstein Barr ◽  
Necrosis Factor

scholarly journals Epstein-Barr Virus Immediate-Early Protein BZLF1 Inhibits Tumor Necrosis Factor Alpha-Induced Signaling and Apoptosis by Downregulating Tumor Necrosis Factor Receptor 1

2004 ◽  
Vol 78 (1) ◽  
pp. 544-549 ◽  
Author(s):  
Thomas E. Morrison ◽  
Amy Mauser ◽  
Aloysius Klingelhutz ◽  
Shannon C. Kenney
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Epstein Barr Virus ◽  
Necrosis Factor Alpha ◽  
Barr Virus ◽  
Early Protein ◽  
Tnf Α ◽  
Factor Alpha ◽  
Epstein Barr ◽  
Necrosis Factor

ABSTRACT Tumor necrosis factor alpha (TNF-α) is a key mediator of host immune and inflammatory responses and inhibits herpesvirus replication by cytolytic and noncytolytic mechanisms. TNF-α effects are primarily mediated through the major TNF-α receptor, TNF-R1, which is constitutively expressed in most cell types. Here we show that the Epstein-Barr virus (EBV) immediate-early protein BZLF1 prevents TNF-α activation of target genes and TNF-α-induced cell death. These effects are mediated by down-regulation of the promoter for TNF-R1. Additionally, we demonstrate that expression of TNF-R1 is downregulated during the EBV lytic replication cycle. Thus, EBV has developed a novel mechanism for evading TNF-α antiviral effects during lytic reactivation or primary infection.

scholarly journals Identification of a novel cyclosporin-sensitive element in the human tumor necrosis factor alpha gene promoter.

1993 ◽  
Vol 178 (4) ◽  
pp. 1365-1379 ◽  
Author(s):  
A E Goldfeld ◽  
P G McCaffrey ◽  
J L Strominger ◽  
A Rao
Keyword(s):  
T Cells ◽  
Protein Synthesis ◽  
T Cell ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Activated T Cells ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Alpha Gene ◽  
Necrosis Factor

Tumor necrosis factor alpha (TNF-alpha), a cytokine with pleiotropic biological effects, is produced by a variety of cell types in response to induction by diverse stimuli. In this paper, TNF-alpha mRNA is shown to be highly induced in a murine T cell clone by stimulation with T cell receptor (TCR) ligands or by calcium ionophores alone. Induction is rapid, does not require de novo protein synthesis, and is completely blocked by the immunosuppressant cyclosporin A (CsA). We have identified a human TNF-alpha promoter element, kappa 3, which plays a key role in the calcium-mediated inducibility and CsA sensitivity of the gene. In electrophoretic mobility shift assays, an oligonucleotide containing kappa 3 forms two DNA protein complexes with proteins that are present in extracts from unstimulated T cells. These complexes appear in nuclear extracts only after T cell stimulation. Induction of the inducible nuclear complexes is rapid, independent of protein synthesis, and blocked by CsA, and thus, exactly parallels the induction of TNF-alpha mRNA by TCR ligands or by calcium ionophore. Our studies indicate that the kappa 3 binding factor resembles the preexisting component of nuclear factor of activated T cells. Thus, the TNF-alpha gene is an immediate early gene in activated T cells and provides a new model system in which to study CsA-sensitive gene induction in activated T cells.

scholarly journals Tumor necrosis factor alpha gene regulation in activated T cells involves ATF-2/Jun and NFATp.

1996 ◽  
Vol 16 (2) ◽  
pp. 459-467 ◽  
Author(s):  
E Y Tsai ◽  
J Jain ◽  
P A Pesavento ◽  
A Rao ◽  
A E Goldfeld
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Gene Transcription ◽  
Tumor Necrosis ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Alpha Gene ◽  
Necrosis Factor

The human tumor necrosis factor alpha (TNF-alpha) gene is one of the earliest genes expressed upon the activation of a T or B cell through its antigen receptor. Previous experiments have demonstrated that in stimulated T cells, a TNF-alpha promoter element, kappa 3, which binds NFATp, is required for the cyclosporin A-sensitive transcriptional activation of the gene. Here, we demonstrate that a cyclic AMP response element (CRE), which lies immediately upstream of the kappa 3 site, is also required for induction of TNF-alpha gene transcription in T cells stimulated by calcium ionophore or T-cell receptor ligands. The CRE binds ATF-2 and Jun proteins in association with NFATp bound to kappa 3. These proteins bind noncooperatively in vitro; however, the transcriptional activity of the CRE/kappa 3 composite site is dramatically higher than the activity of the kappa 3 site alone, indicating that the two sites cooperate in vivo. This study is the first demonstration of a role for ATF-2 in TNF-alpha gene transcription and of a functional interaction between ATF-2/Jun and NFATp. This novel pairing of NFATp with ATF-2/Jun may account for the specific and immediate pattern of TNF-alpha gene transcription in stimulated T cells.

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