Effects of interferon-?, interleukin-1?, and tumor necrosis factor-? on the serotonin metabolism in the nucleus raphe dorsalis of the rat

1997 ◽  
Vol 104 (10) ◽  
pp. 981-991 ◽  
Author(s):  
H. W. Clement ◽  
J. Buschmann ◽  
S. Rex ◽  
C. Grote ◽  
C. Opper ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Serotonin Metabolism ◽  
Raphe Dorsalis ◽  
Necrosis Factor

Pancreatic beta-cell-selective production of tumor necrosis factor-alpha induced by interleukin-1

Diabetes ◽  
1993 ◽  
Vol 42 (7) ◽  
pp. 1026-1031 ◽  
Author(s):  
K. Yamada ◽  
N. Takane ◽  
S. Otabe ◽  
C. Inada ◽  
M. Inoue ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Beta Cell ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Pancreatic Beta Cell ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

scholarly journals Interdependence between Interleukin-1 and Tumor Necrosis Factor Regulates TNF-Dependent Control of Mycobacterium tuberculosis Infection

Immunity ◽  
2015 ◽  
Vol 43 (6) ◽  
pp. 1125-1136 ◽  
Author(s):  
Nelson C. Di Paolo ◽  
Shahin Shafiani ◽  
Tracey Day ◽  
Thalia Papayannopoulou ◽  
David W. Russell ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Tuberculosis Infection ◽  
Mycobacterium Tuberculosis Infection ◽  
Necrosis Factor

Serum tumor necrosis factor and interleukin 1 in leprosy and during lepra reactions

1992 ◽  
Vol 63 (1) ◽  
pp. 23-27 ◽  
Author(s):  
Shreemanta K. Parida ◽  
Georges E. Grau ◽  
S.Ahmed Zaheer ◽  
Rama Mukherjee
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Necrosis Factor ◽  
Serum Tumor Necrosis

scholarly journals Transcription, not synthesis, of interleukin-1 and tumor necrosis factor by complement

1990 ◽  
Vol 37 (1) ◽  
pp. 85-93 ◽  
Author(s):  
Ralf Schindler ◽  
Gerhard Lonnemann ◽  
Stanley Shaldon ◽  
Karl-M. Koch ◽  
Charles A. Dinarello
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Necrosis Factor

scholarly journals Differentiation factor/leukemia inhibitory factor protection against lethal endotoxemia in mice: synergistic effect with interleukin 1 and tumor necrosis factor.

1992 ◽  
Vol 175 (4) ◽  
pp. 1139-1142 ◽  
Author(s):  
H R Alexander ◽  
G G Wong ◽  
G M Doherty ◽  
D J Venzon ◽  
D L Fraker ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Leukemia Inhibitory Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Inhibitory Factor ◽  
Dependent Manner ◽  
Lps Challenge ◽  
Differentiation Factor ◽  
Dose Dependent ◽  
Necrosis Factor

Differentiation factor (D factor), also called leukemia inhibitory factor (LIF), is a glycoprotein that has been increasingly recognized to possess a wide range of physiological activities. We examined the possibility that the administration of D factor may confer beneficial effects and enhance host resistance against lethal endotoxemia. A single intravenous dose of recombinant human D factor completely protected C57/Bl6 mice from the lethal effect of Escherichia coli endotoxin (lipopolysaccharide [LPS]). The protective effects were dose dependent and observed when administered 2-24 h before LPS. Previous work has shown that interleukin 1 (IL-1) and tumor necrosis factor (TNF) also protect against a subsequent LPS challenge in a dose-dependent manner. When human D factor was combined with sub-protective doses of IL-1 beta or TNF-alpha, there was dramatic synergistic protection against a subsequent lethal LPS challenge.

NF-IL6 and AP-1 cooperatively modulate the activation of the TSG-6 gene by tumor necrosis factor alpha and interleukin-1

1994 ◽  
Vol 14 (10) ◽  
pp. 6561-6569
Author(s):  
L Klampfer ◽  
T H Lee ◽  
W Hsu ◽  
J Vilcek ◽  
S Chen-Kiang
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Human Fibroblasts ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Normal Human ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1) activate transcription of the TSG-6 gene in normal human fibroblasts through a promoter region (-165 to -58) that encompasses an AP-1 and a NF-IL6 site. We show by deletion analysis and substitution mutagenesis that both sites are necessary for activation by TNF-alpha. Activation by IL-1 requires the NF-IL6 site and is enhanced by the AP-1 site. These results suggest that the NF-IL6 and AP-1 family transcription factors functionally cooperate to mediate TNF-alpha and IL-1 signals. Consistent with this possibility, IL-1 and TNF-alpha markedly increase the binding of Fos and Jun to the AP-1 site, and NF-IL6 activates the native TSG-6 promoter. Activation by NF-IL6 requires an intact NF-IL6 site and is modulated by the ratio of activator to inhibitor NF-IL6 isoforms that are translated from different in-frame AUGs. However, the inhibitor isoform can also bind to the AP-1 site and repress AP-1 site-mediated transcription. The finding that the inhibitor isoform antagonizes activation of the native TSG-6 promoter by IL-1 and TNF-alpha suggests that NF-IL6 has a physiologic role in these cytokine responses. Thus, the functionally distinct NF-IL6 isoforms cooperate with Fos and Jun to positively and negatively regulate the native TSG-6 promoter by TNF-alpha and IL-1.

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