Cyclin A and CDK2 Kinase-Activity Are Suppressed by Combined Treatment with Tumor Necrosis Factor-α and Interferon-α

1995 ◽  
Vol 213 (3) ◽  
pp. 1115-1121 ◽  
Author(s):  
K. Satomoto ◽  
M. Haisa ◽  
Y. Naomoto ◽  
N. Tanaka ◽  
K. Orita
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Kinase Activity ◽  
Combined Treatment ◽  
Cyclin A ◽  
Interferon Α ◽  
Factor Α ◽  
Necrosis Factor

Effect of interferon α, γ, and tumor necrosis factor α on the HLA-A, B, C expression of cell lines derived from human liver

2008 ◽  
Vol 9 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Kentaro Yoshioka ◽  
Shinichi Kakumu ◽  
Hirofumi Tahara ◽  
Motohiro Arao ◽  
Akihiko Fuji
Keyword(s):  
Tumor Necrosis Factor ◽  
Cell Lines ◽  
Human Liver ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interferon Α ◽  
Factor Α ◽  
Necrosis Factor

Interaction of interferon-α with interleukin-1β or tumor necrosis factor-α on hepatitis B virus enhancer activity

1992 ◽  
Vol 183 (2) ◽  
pp. 904-909 ◽  
Author(s):  
Keisuke Hamasaki ◽  
Keisuke Nakata ◽  
Kazuhiko Nakao ◽  
Satoru Mitsuoka ◽  
Takuya Tsutsumi ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Tumor Necrosis Factor ◽  
Hepatitis B ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interferon Α ◽  
Enhancer Activity ◽  
B Virus ◽  
Factor Α ◽  
Necrosis Factor

Verotoxin 1 from Escherichia coli Affects Gb3/CD77+ Bovine Lymphocytes Independent of Interleukin-2, Tumor Necrosis Factor-α, and Interferon-α

2003 ◽  
Vol 228 (4) ◽  
pp. 377-386 ◽  
Author(s):  
Christian Menge ◽  
Ivonne Stamm ◽  
Maike Blessenohl ◽  
Lothar H. Wieler ◽  
Georg Baljer
Keyword(s):  
Escherichia Coli ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Interleukin 2 ◽  
Γδ T Cells ◽  
Interferon Α ◽  
Bovine Lymphocytes ◽  
Factor Α ◽  
Necrosis Factor

Verotoxin (VT)-induced immunomodulation has been implicated in the ability of VT-producing Escherichia coli (VTEC) to cause persistent infections in cattle. VT1, also referred to as Shiga toxin 1, is a potent cytotoxin that modulates cytokine secretions and functions. This prompted the current investigation to examine whether the inhibiting effect of VT1 on bovine lymphocytes correlates with the expression of the cellular VT1 receptor Gb3/CD77 or is mediated instead via perturbation of cytokine secretion. Using blood mononuclear cells stimulated by mitogens as a model, VT1 significantly blocked lymphoblast transformation and proliferation in the BoCD8+ T cell and BoCD21+ B cell population. In contrast, VT1 dramatically reduced the number of viable Gb3/CDTZ+ blast cells within all subpopulations identified (BoCD2+, BoCD4+, BoCD8+, WC1+ [i.e., γδ T cells] BoCD21+, and BoCD25+). Similar effects of VT1 were observed when the culture medium was supplemented with selected cytokines: tumor necrosis factor-α-sensitizing endothelial cells against VT1, interferon-a (IFN-α) as bovine IFN-α receptors are partially homologous to the B-subunit of VT1, and interleukin-2 that is critical for lymphocyte proliferation in vitro. The addition of these cytokines was neither able to mimic nor to overcome the effects of VT1. Therefore, it is concluded that VT1 directly acts on bovine lymphocytes rather than inducing a cytokine-mediated effect. VT1 considerably affects all main bovine lymphocyte subpopulations, implicating that the immune system is a predominant target for VT1 In cattle.

Sign in / Sign up

Export Citation Format

Share Document